Academic literature on the topic 'Low t cell symptoms'
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Journal articles on the topic "Low t cell symptoms"
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Milani, C., and J. Castillo. "HIV-associated peripheral T-cell lymphoma." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e19551-e19551. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e19551.
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e19551 Background: T-cell lymphomas (TCL) constitute 3% of all AIDS-related lymphomas. Over the past 2 decades numerous case reports have documented the emergence of TCL among HIV-infected individuals. These lymphomas comprise a diverse group of disease entities, including peripheral T-cell lymphomas (PTCL), which represent the most common subtype. The aim of this study was to investigate the clinical and pathological features of HIV-associated PTCL. Methods: A MEDLINE search for cases of HIV-associated PTCL was conducted through December 2008. Data regarding patient age, gender, HIV status (CD4 count, viral load, opportunistic infections), use of HAART, lymphoma features (B symptoms, stage, sites of involvement, immunophenotype, molecular studies), EBV coinfection, therapy, and outcome (survival, cause of death) were analyzed and reported descriptively. Results: A total of 34 cases were included. Patients had a median age of 36 years with a male:female ratio of 4:1. Median CD4+ count was 126 cells/mm3. Seventeen patients (50%) had an opportunistic infection, but only 7 patients (26%) were on HAART treatment; 4 patients on HAART (57%) were alive at time of publication. PTCL was extranodal in 75% of cases, affecting predominantly the oral cavity, lung, and GI tract. B symptoms were present in 60% of cases. Stage III and IV disease was found in 17 and 5 cases, respectively, accounting for 76% of the total cases. T-cell receptor gene rearrangement was positive in 10 out of 10 (100%) analyzed cases. EBV was identified in 6 of 12 cases (50%). Median LDH level was 269 IU/L. Therapy for PTCL was administered in 23 cases (68%), while 10 cases (30%) did not receive therapy; 9 of the treated patients (39%) received CHOP with a 33% remission rate. Twenty-two patients (69%) died complicated by infections in 57% and lymphoma progression in 36% of cases. The reported median survival was 12 months. Conclusions: HIV-associated PTCL tends to affect young male individuals with low CD4 counts. Apart from marked immunosuppression, the poor prognosis of HIV-associated PTCL appears to be related to advanced stage at presentation, presence of B symptoms, elevated LDH levels, prominent extranodal disease, and poor response to CHOP chemotherapy. The role of HAART and EBV in the development of PTCL needs further clarification. No significant financial relationships to disclose.
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Klameth, Andreas, Andreas Neubauer, Christian Keller, Christian Aepinus, Ulrich Kaiser, Jörg Hoffmann, and Cornelia Brendel. "Aberrant CD3-Positive, CD8-Low, CD7-Negative Lymphocytes May Appear During Viral Infections and Mimic Peripheral T-Cell Lymphoma." Diagnostics 10, no. 4 (April 7, 2020): 204. http://dx.doi.org/10.3390/diagnostics10040204.
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Flow cytometry (FC) facilitates diagnosis of peripheral T-cell non-Hodgkin lymphoma (T-NHL), but overlapping features between reactive and neoplastic T-cell proliferations often hamper a rapid assessment. One hundred forty peripheral blood samples submitted to diagnostic FC for T-cell immunophenotyping were retrospectively analyzed. A T-cell population with a conspicuous aberrant surface epitope expression pattern was observed in 18 cases and diagnostic follow up was performed. The aberrant T-cell population exhibited a low scatter profile, a CD7-negative/low, CD8-low and CD3-positive immunophenotype, and monoclonal T-cell receptor expansion. T-NHL was ruled out by follow up in all cases. Epstein-Barr virus infection was diagnosed in 12 cases, cytomegalovirus infection in three cases; one patient had been vaccinated. The irregular subpopulation disappeared spontaneously within days or weeks. We describe a novel peripheral blood T-cell subpopulation with a low light scatter and CD8-low, CD7-negative/low and CD3-positive marker expression profile, which indicates reactive T-cell expansion in patients who present with peripheral lymphadenopathy and/or B symptoms.
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Baaij, Laura R. de, Jolanda MW van de Water, Wieke HM Verbeek, Otto J. Visser, Dirk J. Kuik, Joost J. Oudejans, Chris JLM Meijer, Chris JJ Mulder, and Saskia AGM Cillessen. "Enteropathy-Associated T-Cell Lymphoma: a Clinical Prognostic Model to Identify High Risk Patients." Blood 116, no. 21 (November 19, 2010): 3092. http://dx.doi.org/10.1182/blood.v116.21.3092.3092.
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Abstract Abstract 3092 Enteropathy-associated T-cell lymphoma (EATL) is a rare intestinal lymphoma that arises from intraepithelial lymphocytes. In Western countries EATL accounts for 5% of all gastrointestinal lymphomas and in 80–90% of all cases this lymphoma is associated with celiac disease (CD). Based on clinical presentation, EATL can be divided into two subtypes: primary and secondary EATL. Primary EATL develops without a preceding history of CD. The first presentation is often perforation or obstruction, which leads to diagnosis of both EATL and CD. Secondary EATL is diagnosed in patients with well-established CD or refractory CD. These patients deteriorate and eventually develop EATL. The current standard treatment for both types of EATL consists of surgery and chemotherapy, but overall survival (OS) is poor and new therapeutic strategies are urgently needed. For risk-based selection of patients for new therapies and clinical trials, prognostic models as the International Prognostic Index (IPI) are generally used. Since IPI is not predictive for EATL, we determined a prognostic model specifically for EATL, which can identify high-risk patients who need more aggressive therapy. Forty-one patients were diagnosed with EATL and retrospectively analyzed. Two- and 5-years OS were 18% and 10% respectively (range: 0 – 97 months). In multivariate analysis, 3 risk factors were predictive for survival: serum LDH > normal (P < 0.001; RR 6.65; 95% CI 1.96 to 9.89), presence of B-symptoms (P < 0.001; RR 4.41; 95% CI 2.73 to 16.18) and subtype secondary EATL (P = 0.036; RR 2.33; 95% CI 1.06 to 5.13). A weighted point score was assigned to each of these 3 factors and a prognostic model was constructed. Four risk groups were identified (P < 0.0001). Group I showed most favorable outcome: 2- and 5-years OS were 55% and 30% respectively. Although survival rates in groups II, III and IV were significantly different, in none of these groups 2-years survival was achieved. Therefore, the model was simplified to a low risk and a high risk group (P < 0.0001, Figure 1). The low risk group represented patients with no risk factors, i.e. primary EATL with no B-symptoms and normal LDH. In the high risk group, patients had 1 or more of the risk factors elevated serum LDH, B-symptoms or subtype secondary EATL. The new prognostic model showed superior predictive capacity as compared to IPI. In conclusion, our new prognostic model clearly identifies a high and a low risk group. Patients with one or more of the risk factors serum LDH > normal, B-symptoms or subtype secondary EATL are at high risk, and therefore new therapies for this group are urgently needed. Figure 1: Survival in EATL. Low risk group = no risk factors. High risk group = presence of 1 or more of the following risk factors: serum LDH > normal, B-symptoms or subtype secondary EATL. Figure 1:. Survival in EATL. Low risk group = no risk factors. High risk group = presence of 1 or more of the following risk factors: serum LDH > normal, B-symptoms or subtype secondary EATL. Disclosures: No relevant conflicts of interest to declare.
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Federico, Massimo, Thomas Rudiger, Monica Bellei, Bharat N. Nathwani, Stefano Luminari, Bertrand Coiffier, Nancy L. Harris, et al. "Clinicopathologic Characteristics of Angioimmunoblastic T-Cell Lymphoma: Analysis of the International Peripheral T-Cell Lymphoma Project." Journal of Clinical Oncology 31, no. 2 (January 10, 2013): 240–46. http://dx.doi.org/10.1200/jco.2011.37.3647.
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PurposeThe International Peripheral T-Cell Lymphoma Project was undertaken to better understand the subtypes of T-cell and natural killer (NK) –cell lymphomas.Patients and MethodsAngioimmunoblastic T-cell lymphoma (AITL) was diagnosed according to the 2001 WHO criteria by a central review process consisting of panels of expert hematopathologists. Clinical, pathologic, immunophenotyping, treatment, and survival data were correlated.ResultsOf 1,314 patients, 243 (18.5%) were diagnosed with AITL. At presentation, generalized lymphadenopathy was noted in 76% of patients, and 89% had stages III to IV disease. Skin rash was observed in 21% of patients. Hemolytic anemia and hypergammoglobulinemia occurred in 13% and 30% of patients, respectively. Five-year overall and failure-free survivals were 33% and 18%, respectively. At presentation, prognostic models were evaluated, including the standard International Prognostic Index, which comprised the following factors: age ≥ 60 years, stages III to IV disease, lactic dehydrogenase (LDH) > normal, extranodal sites (ENSs) > one, and performance status (PS) ≥ 2; the Prognostic Index for Peripheral T-Cell Lymphoma, comprising: age ≥ 60 years, PS ≥ 2, LDH > normal, and bone marrow involvement; and the alternative Prognostic Index for AITL (PIAI), comprising: age > 60 years, PS ≥ 2, ENSs > one, B symptoms, and platelet count < 150 × 109/L. The simplified PIAI had a low-risk group (zero to one factors), with 5-year survival of 44%, and a high-risk group (two to five factors), with 5-year survival of 24% (P = .0065).ConclusionAITL is a rare clinicopathologic entity characterized by an aggressive course and dismal outcome with current therapies.
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Gerevini, Simonetta, Ruggero Capra, Diego Bertoli, Alessandra Sottini, and Luisa Imberti. "Immune profiling of a patient with alemtuzumab-associated progressive multifocal leukoencephalopathy." Multiple Sclerosis Journal 25, no. 8 (April 9, 2019): 1196–201. http://dx.doi.org/10.1177/1352458519832259.
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A 31-year-old woman affected by multiple sclerosis (MS) experienced generalized tonic–clonic seizures 2 months after the second alemtuzumab cycle. Positive JC virus (JCV)-DNA in cerebrospinal fluid (CSF) and lesion iconography at magnetic resonance imaging (MRI) were suggestive of progressive multifocal leukoencephalopathy (PML). After 1 month, during full-blown immune reconstitution inflammatory syndrome, JCV-DNA became negative and symptoms gradually improved. New T- and B-cell output and T- and B-cell diversity were low and lymphocytes poorly responded to stimulation. This is the first case of an alemtuzumab-treated patient with clinical symptoms and radiological features compatible with PML. The lack of large T- and B-cell diversity, necessary for JCV recognition, is likely to have concurred to PML insurgence.
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Endo, Tomonori, Daiya Asaka, Tsuguhisa Nakayama, Shota Saito, Hiroki Kodama, Ryoto Mitsuyoshi, Naoki Sugimoto, et al. "Long-term oral administration of transgenic rice containing cedar pollen T-cell epitopes potentially improves medication- and allergy-related quality-of-life scores." Allergy and Asthma Proceedings 42, no. 4 (July 1, 2021): 293–300. http://dx.doi.org/10.2500/aap.2021.42.210011.
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Background: We previously developed a transgenic rice that contains seven linked human predominant T-cell epitopes (7Crp) derived from Japanese cedar (JC) pollen allergens Cry j 1 and Cry j 2. Oral administration of 80 g of transgenic rice for 20 weeks suppressed allergen-specific T-cell proliferation in participants with JC pollinosis, but their clinical symptoms did not improve. Objective: We examined the clinical efficacy of low-dose (5 g and 20 g) intake of the transgenic rice administered for two successive seasons. Methods: In this randomized, double-blind, placebo controlled study, transgenic rice seeds (5 g or 20 g) were orally administered to the participants for 24 weeks in each of two successive JC pollen seasons. We analyzed T-cell proliferation and cytokine expression, and monitored symptom and medication scores during the pollen season. Quality of life (QOL) was evaluated by using the Japanese Allergic Rhinitis Quality of Life Standard Questionnaire (JRQLQ). Results: Specific T-cell proliferation after stimulation with 7Crp, Cry j 1, and Cry j 2 was significantly suppressed in the second JC pollen season. No significant differences were found among the three groups (5 g, 20 g, and placebo) with regard to clinical symptoms or medication scores in the first season. However, the medication scores and face scale for overall condition of JRQLQ improved in the 5-g transgenic rice group in the second season, although careful re-examination with a large sample size is necessary to confirm the results. Conclusion: Low-dose oral administration of transgenic rice that contains 7Crp significantly reduced allergen-specific T-cell responses and improved medication scores during the second season of administration. Thus, oral intake of the transgenic rice has the potential to induce immune tolerance to JC pollen allergens when administered for at least two successive seasons.
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Slovick, Anna, Abdel Douiri, Rachel Muir, Andrea Guerra, Konstantinos Tsioulos, Evie Haye, Emily PS Lam, et al. "A randomised placebo-controlled trial investigating efficacy and mechanisms of low-dose intradermal allergen immunotherapy in treatment of seasonal allergic rhinitis." Efficacy and Mechanism Evaluation 3, no. 10 (December 2016): 1–80. http://dx.doi.org/10.3310/eme03100.
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BackgroundWe previously reported that repeated low-dose grass pollen intradermal allergen injection suppresses allergen-induced cutaneous late-phase responses, comparable with conventional high-dose subcutaneous and sublingual immunotherapy.ObjectiveTo evaluate the efficacy and mechanism of grass pollen intradermal immunotherapy for treatment of allergic rhinitis.DesignA Phase II, double-blind, randomised controlled parallel-group trial.SettingSingle-centre UK study.ParticipantsAdults aged 18–65 years, with grass pollen-induced allergic rhinoconjunctivitis.InterventionsSeven 2-weekly intradermal injections were given into the forearm, containing eitherPhleum pratensesoluble grass pollen extract (7 ng of the major allergen Phl p 5) or histamine control.Main outcome measuresThe primary outcome was a combined symptom and medication score (CSMS) during the 2013 grass pollen season. Secondary clinical outcomes were overall symptom scores; individual symptoms scores for nose, mouth, eyes and lungs; overall medication scores; CSMSs during the peak season; visual analogue scale (VAS) scores for nose and eye symptoms; Mini Rhinitis Quality of Life Questionnaire scores; health-related quality-of-life scores (European Quality of Life-5 Dimensions, 5-levels); a global evaluation of symptoms, number of symptom-free and medication-free days; number of days when prednisolone was used; and adverse events. Mechanistic studies included measurement of late-phase skin response sizes, allergen-specific antibody titres, analysis of skin biopsies and basophil activation tests.ResultsThere was no significant difference in CSMSs between treatment arms [difference in median area under curve (AUC) 14, 95% confidence interval (CI) –172.5 to 215.1;p = 0.80]. Paradoxically, among the secondary outcomes, nasal symptoms measured with daily scores were higher in the active arm (difference in median AUC 35, 95% CI 4.0 to 67.5;p = 0.03), with a trend for higher nasal symptoms measured by VASs (difference in median AUC 53, 95% CI –11.6 to 125.2;p = 0.05). No differences were seen in other clinical outcomes in the main intention-to-treat analysis. In mechanistic studies, active treatment increasedP. pratense-, Phl p 1- and Phl p 5-specific immunoglobulin E (allp = 0.001) compared with the control. T cells cultured from skin biopsies of active intradermal immunotherapy subjects showed higher T helper type 2 cell (Th2) marker CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 cells) expression (p < 0.05) and lower T helper type 1 cell marker CXCR3 [chemokine (C-X-C Motif) receptor 3] expression (p < 0.05), respectively. Interleukin 5 messenger ribonucleic acid, measured by microarray, was more highly expressed by cultured skin T cells in the active arm (p < 0.05). Late-phase skin responses to grass pollen were still inhibited up to 7 months after intradermal immunotherapy (p = 0.03), but not at 10–13 months’ time points.LimitationsGrass pollen doses were not increased during the course, as our proof-of-concept trial showed that repeating the same doses was sufficient to achieve almost complete late-response suppression. Injections were not continued throughout the season, as previous subcutaneous grass pollen immunotherapy trials have demonstrated preseasonal regimen efficacy.ConclusionsIntradermal immunotherapy suppressed late-phase skin responses to allergen, but was not clinically effective. The intervention appeared to have an immunological priming effect and exacerbated certain seasonal symptoms, notably in the nose.Future workFurther studies on low-dose intradermal grass pollen immunotherapy are not recommended because of our demonstrated worsening of allergic rhinitis symptoms and immunological priming. The findings are of great significance for other novel immunotherapies targeting the skin, such as epicutaneous techniques.Trial registrationCurrent Controlled Trials ISRCTN78413121.FundingThis project was funded by the Efficacy and Mechanism Evaluation programme, a Medical Research Council and National Institute for Health Research partnership.
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Autio, Matias, Suvi-Katri Leivonen, Teijo Pellinen, and Sirpa Leppa. "Clinical Impact of Tumor-Associated Macrophage and T-Cell Contents in Diffuse Large B-Cell Lymphoma." Blood 136, Supplement 1 (November 5, 2020): 33. http://dx.doi.org/10.1182/blood-2020-142331.
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Background: Tumor infiltrating immune cells can modulate cancer progression and are attractive therapeutic targets. We have previously identified a tumor microenvironment (TME) immune cell signature in diffuse large B-cell lymphoma (DLBCL), which contains genes for cytolytic factors, immune checkpoint molecules, T-cells and macrophages, and separates the patients into immune cell high and low or T-cell inflamed and non-inflamed subgroups (Autio et al., 2020). As macrophages and T-cells are key components of the TME, our aim was to characterize their phenotypes and relationships in the tumor tissue and associate the findings to clinical outcome in patients with DLBCL. Methods: We used multiplex immunohistochemistry, gene expression data, and unsupervised computational approaches to characterize tumor associated T-cell and macrophage (TAM) phenotypes in 178 samples from DLBCL patients. We correlated the immune cell constitution with clinical data, and validated the findings utilizing gene expression data from three independent DLBCL cohorts (Reddy et al., 2017, Schmitz et al., 2018, Chapuy et al., 2018) and in silico immunophenotyping with CIBERSORT. Results: The proportions of TAMs and infiltrating T-cells varied significantly between the patients. Unsupervised hierarchical clustering divided the samples into T-cell inflamed and non-inflamed subgroups. The T-cell inflamed phenotype was rich in other immune cell subtypes such as TAMs, natural killer (NK) cells, and regulatory T-cells, thus characterizing an immune hot phenotype. Apart from B-symptoms being more common in the patients with T-cell inflamed phenotype, clinical characteristics were equally distributed between the subgroups, and no association with survival was observed. However, when we divided the T-cell inflamed group further into subgroups according to the TAM content, we identified a T-cell high/macrophage low group, which was characterized by clinically less aggressive disease and better survival as compared to the T-cell high/macrophage high or T-cell low groups. Using in silico deconvolution analyses, we validated the T-cell high/macrophage low subgroup, and its association with less aggressive disease and survival in an external dataset comprising 496 patients (Reddy et al., 2017). The prognostic impact of T-cell high/macrophage low subgroup on survival was independent of the IPI and molecular subtype. Differential gene expression analyses identified a gene signature corresponding to the T-cell high/macrophage low subgroup. This signature translated to better outcome, and was validated in two additional datasets (Schmitz et al. n=562, Chapuy et al. n=137). Finally, we studied the impact of immune checkpoint expressing TAMs on survival, and whether it differed between the T-cell inflamed and T-cell non-inflamed subgroups. In particular, a high proportion of PD-L1+, TIM3+, and PD-L1+TIM3+CD163- macrophages associated with poor outcome, independent from the IPI and molecular subtype. Furthermore, the impact of these TAM subtypes on survival was evident only in the patients with T-cell inflamed phenotype. Conclusions: Our data demonstrate that the proportions of different immune cell phenotypes in the DLBCL TME are clinically meaningful, and suggest that the high T-cell/macrophage ratio predicts favorable survival in patients with DLBCL. Disclosures Leppa: Novartis: Consultancy; Takeda: Consultancy; Celgene: Research Funding; Bayer: Research Funding; Incyte: Consultancy; Roche: Consultancy, Research Funding.
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Huang, Yenlin, Anne Moreau, Jehan Dupuis, Berthold Streubel, Barbara Petit, S. Legouill, Nadine Martin-Garcia, et al. "Peripheral T-Cell Lymphomas with Follicular Growth Patterns Are Derived from Follicular Helper T Cells (TFH): A Link with Angioimmunoblastic T-Cell Lymphomas?." Blood 110, no. 11 (November 16, 2007): 3568. http://dx.doi.org/10.1182/blood.v110.11.3568.3568.
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Abstract Nodal peripheral T-cell lymphomas represent a heterogeneous category, composed of three entities: anaplastic large cell lymphomas, peripheral T-cell lymphomas unspecified (PTCLu) and angioimmunoblastic T-cell lymphomas (AITL). The later entity has been recently recognized to derive from follicular helper T cells (TFH). Among PTCLu - which represents an ill-defined entity - a peculiar form with follicular growth pattern (PTCL-F) has been recently reported, and one article stated their association with t(5 ;9)(q33 ;q22) involving ITK and SYK (Leukemia2006; 20: 313–318). However, the origin of tumor cells and clinical aspects of this group of PTCL-F are still unknown. The aim of this study was to analyse a series of PTCL-F to describe their clinical and histopathological aspects, to identify their cell of origin, and their relationship with AITL. Fourty-two patients from 32 to 85 years of age with 51 biopsies were selected from three Departments of Pathology (Creteil, n=24, Nantes n=13, Vienna n=14). All patients showed histopathologic features of PTCL-F in at least one biopsy. Biopsies were classified into three categories according to predominant morphological features at low power magnification: follicular lymphoma-like (n=7), progressive transformation of germinal center-like (n=22), and AITL-like features with follicular colonization (n=19). Several cases have combinations of patterns. The neoplastic population is characterized by medium-sized cells with clear cytoplasm surrounded by IgD+ B-cells. Tumor cells are of helper T-cell immunophenotype [CD2+ (33/33 = 100%), CD3+ (45/48 = 93%), CD4+ (35/42 = 83%), CD5+ (39/39 = 100%), CD7+ (7/37 = 19%)], with frequent expression of CD10 (29/43 = 67%) and of TFH markers [PDCD-1 (32/36 = 88%), CXCL13+ (33/38 = 87%), BCL6+ (15/25 = 60%), CD57+ (9/16 = 56%)]. Scattered CD20+ B-immunoblasts (27/28 = 96%) and EBV+ cells (18/30 = 60%) are also frequently observed. Seven out of 31 patients (22%) in the 3 morphological patterns have t(5 ;9)(q33 ;q22) detected by fluorescent in situ hybridization. At prentation and/or at relapse, most patients had multiple lymphadenopathies (19/23 = 83%) and disseminated disease (stages III–IV, 22/28 = 79%). Skin lesions and B symptoms were present in 7/19 (37%) and 6/22 (27%) patients, respectively. In addition, 2 patients with sequential biopsies disclosed typical clinical & histopathological features of AITL in one episode. Our results show that this rare form of PTCL has an immunophenotype indicative of TFH origin, is associated with t(5 ;9) in a proportion of cases, shows some similarities in morphology and immunophenotype with AITL, suggesting a relationship, and generates diagnostic pitfalls, especially with atypical reactive lymphoid lesions and some B-cell lymphomas. The use of immunohistochemistry with TFH markers and molecular studies can help to make a correct diagnosis.
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Reimer, Peter, Thomas Ruediger, Florian Weissinger, Hans Konrad Mueller-Hermelink, Andreas Engert, Hermann Einsele, and Martin Wilhelm. "Different Outcome for Angioimmunoblastic T-Cell Lymphoma (AIL) and Peripheral T-Cell Lymphoma Unspecified (PTCL-U) Following Upfront Autologous Stem Cell Transplantation." Blood 108, no. 11 (November 16, 2006): 5431. http://dx.doi.org/10.1182/blood.v108.11.5431.5431.
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Abstract Introduction: Peripheral T-cell lymphomas (PTCL) are rare diseases and optimal treatment strategies still remain to be defined. With the exception of the ALK-positive anaplastic large cell lymphoma (ALCL) that shows a favourable outcome following conventional chemotherapy, PTCL are known for their poorer prognosis compared to aggressive B-cell lymphomas. However, the impact of the different PTCL-subtypes on treatment outcome has not been clearly demonstrated in prospective studies. PTCL unspecified (PTCL-U) and angioimmunoblastic T-cell lymphoma (AIL) represent the most common subtypes of PTCL in Western countries, accounting for approximately 70% of PTCL. We therefore analysed the data of our study on myeloablative radiochemotherapy followed by autologous stem cell transplantation (ASCT) in primary diagnosed PTCL with regard to the main histologic subtypes. Material and Methods: From 06/00 to 06/06 92 patients with confirmed diagnosis of PTCL entered the study. Primary cutaneous PTCL and ALK+ ALCL were excluded from the trial. Main subtypes were PTCL-U (n= 37) and AIL (n= 28) accounting for 65 of the 92 patients (71%). 0f these patients 53 (PTCL, n= 31; AIL, n= 22) were evaluable for the analysis (82%). Results: Median age was 50 years in the PTCL-U and 47.5 years in the AIL group, respectively. The International Prognostic Index (IPI) did not differ in both groups. In the PTCL-U and the AIL group a low/intermediate-low risk was found in 35% and 36%, respectively and a high/intermediate-high risk in 65% and 64%, respectively. There were slightly more patients in stage IV in the AIL group compared to the PTCL-U group (64% versus 53%). In addition, more patients in the AIL group complained of B-symptoms and had bone marrow involvement compared to the PTCL-U group (86% versus 66% and 48% versus 39%, respectively). However, in an intent-to treat analysis only 58% in the PTCL-U group compared to 82% in the AIL group underwent ASCT mainly due to a higher rate of patients with progressive disease in the PTCL-U group. The median overall survival (OS) was 11 months in the PTCL-NOS and 20 months in the AIL group. Regarding only patients undergoing ASCT, the median OS was 13.5 months in the PTCL-U and 25.5 months in the AIL group. Conclusion: Our analysis suggests that patients with AIL, although showing a slightly more unfavourable risk profile at diagnosis, benefit more from upfront autotransplantation than patients with PTCL-U in our study.
Dissertations / Theses on the topic "Low t cell symptoms"
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Deaver, Darcie Marie. "Predictors of Quality of Life in Patients with Cutaneous T cell Lymphoma." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4883.
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Abstract
Cutaneous T cell lymphoma (CTCL) is a rare, incurable, chronic disease accounting for approximately 3% of non-Hodgkin's lymphoma diagnoses every year. Patients with CTCL have skin lesions that can vary in severity putting patients at risk for developing symptoms that may impair their quality of life (QOL). The disease burden can lead to increased depressive symptoms, fatigue distress, and anxiety that the disease may be worsening. Seventy-five participants agreed to take part in an exploratory, prospective study to evaluate depressive symptoms, anxiety, fatigue distress, and spirituality as predictors of QOL in CTCL patients. Demographic variables including stage of disease, ethnicity, age, gender, marital status, level of education, and time since diagnosis, were also included in the analyses to assess for relationships. Bivariate correlations, t-tests, and regression analyses were conducted to assess for relationships among the predictor variables and QOL. The analyses revealed that the proposed model explained 64% of the variance, and depressive symptoms (t= -2.4, p= 0.020) and stage of disease (t= -3.0, p= 0.004) significantly predicted the QOL of CTCL patients. Evaluating for predictors that influence the QOL helps us to better understand the needs of the patients afflicted with CTCL. The importance of studying the QOL of the CTCL patients lies in the fact that nurses can assist in helping patients alleviate some of the symptoms they experience, thereby improving their QOL. Further study is warranted in developing interventions to assist in the preservation of QOL.
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Wurm, Marion Irene [Verfasser]. "Evaluation of T cell response to native and oxidized low- density lipoprotein ( LDL) in atherosclerosis / Marion Irene Wurm." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1025238923/34.
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Touzart, Aurore. "Leucémies aigüs lymphoblastiques T (LAL-T) et dérégulation épigénétique Site- and allele-specific polycomb dysregulation in T-cell leukaemia Epigenetic silencing affects L-asparaginase sensitivity and predicts outcome in T-ALL Low level CpG island promoter methylation predicts a poor outcome in adult T-ALL." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB221.
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Les LAL-T sont des proliférations malignes de précurseurs lymphoïdes T bloqués à un stade précis de leur maturation. Si les anomalies génétiques impliquées dans la leucémogenèse T sont de mieux en mieux connues, les modifications de la régulation épigénétique sont beaucoup moins étudiées. Mon travail de thèse a consisté à étudier la dérégulation épigénétique intervenant dans les LAL-T au travers de 3 projets principaux. Dans le premier travail, nous avons identifié un mécanisme original de dérégulation de l’oncogène TAL1 consistant en la création d’un « neo-enhancer » oncogénique. TAL1 est l’un des oncogènes les plus fréquemment dérégulés dans les LAL-T. Cette dérégulation résulte principalement de translocations avec le locus du TCR ou des micro-délétions interstitielles SIL-TAL1, anomalies chromosomiques altérant des éléments de cis-régulation engendrant une expression ectopique monoallélique de TAL1. Mais dans une proportion importante de cas (environ 50%) de LAL-T TAL1+, une expression aberrante de TAL1 est observée sans que le mécanisme en cause ne soit identifié suggérant l’existence de mécanismes génétiques ou épigénétiques non connus. Nous avons découvert une nouvelle anomalie somatique consistant en une micro-insertion focale et récurrente 7 kpb en amont de TAL1, dans une région intergénique non-codante, responsable de la création d’un « neo-enhancer » oncogénique accompagné d’une modification des marques épigénétiques d’histones i.e. une substitution des marques répressives H3H27me3 par des marques activatrices H3K27ac. Ces micro-insertions sont un événement récurrent dans les LAL-T et ont été retrouvées dans 20% des LAL-T TAL1+ inexpliquées. Au travers du deuxième projet, j’ai tenté de mieux comprendre les bases biologiques à l’origine de différences de réponse au traitement. En effet, considérant deux groupes oncogéniques proches, le pronostic des patients TLX1+, déjà plutôt favorable dans le protocole LALA-94, n’a pas été significativement amélioré dans le protocole thérapeutique intensifié d’inspiration pédiatrique GRAALL 2003-2005 alors que les patients TLX3+ semblent avoir particulièrement bénéficié de ce dernier; les deux protocoles différant majoritairement par les doses de L-asparaginase. Nous avons montré que les patients TLX1+ exprimaient moins d’ASNS (Asparagine synthétase) que les patients TLX3+ et TLX- et que cette moindre expression résultait d’une inhibition épigénétique d’ASNS, à la fois par méthylation du promoteur et diminution des marques histones activatrices. Un niveau de méthylation d’ASNS bas est par ailleurs associé à une moindre sensibilité in vitro à la L-asparaginase. Enfin, la méthylation d’ASNS est un facteur pronostic indépendant pour les patients inclus dans le protocole GRAALL 2003-2005 suggérant que le statut de la méthylation d’ASNS au diagnostic pourrait intervenir dans l’adaptation des doses de L-asparaginase. Dans le troisième projet, je me suis intéressée à la méthylation globale de l’ADN. L’étude de la méthylation par MeDIP-array d’une série de 24 LAL-T nous a permis d’identifier des signatures de méthylation différentielle et de définir un panel minimum de 9 promoteurs de gènes dont l’étude de la méthylation par MS-MLPA a permis de déterminer un ratio de méthylation pour une large série de LAL-T adultes du GRAALL 2003-2005. Le statut de méthylation semble dicté par l’oncogène dérégulé avec en particulier les LAL-T TLX1+ ou TLX3+ associées à une signature d’hyperméthylation et les LAL-T SIL-TAL1+ à une signature d’hypométhylation. Ce statut de méthylation est par ailleurs un facteur pronostique indépendant. Ainsi, les patients hypométhylés ont un pronostic significativement plus défavorable que les patients hyperméthylés. Ensemble, ces résultats illustrent comment des perturbations de la régulation épigénétique peuvent intervenir à la fois dans l’oncogénèse des LAL-T mais aussi dans la réponse au traitementT-ALLs are rare lymphoid neoplasms characterized by the proliferation of immature T precursors arrested at specific stages of maturation. While the genetic abnormalities involved in T-ALL leukemogenesis are becoming better known, alterations in epigenetic regulation, a very important component of the cellular homeostasis, are much less studied. My work was to tsudy the epigenetic deregulation in T-ALL through 3 main projects. In the first project, we identified an original mechanism of TAL1 oncogene deregulation. TAL1 is one of the most frequently deregulated oncogenes in T-ALL. This deregulation results mainly from translocations with the TCRδ locus or micro-deletions SIL-TAL1, two chromosomal abnormalities altering cis-regulatory elements leading to monoallelic TAL1 expression. But in a significant proportion of cases (about 50%) of TAL1+ T-ALL, an aberrant expression of TAL1 is observed without recognized mechanism suggesting unknown genetic or epigenetic mechanisms. We discovered a new somatic alteration consisting of a focal and recurrent microinsertion 7 kbp upstream of TAL1, in a non-coding intergenic region, responsible for the creation of an oncogenic "neo-enhancer" accompanied by a modification of epigenetic histone marks i.e. a “switch” from H3H27me3 repressive marks to H3K27ac activating marks. These microinsertions are a recurrent event in T-ALL and have been found in 20% of “unresolved” TAL1+ T-ALL. Through the second project, I tried to better understand the biological bases for discrepancies in patients related response to treatment. Indeed, considering two close oncogenic groups, the prognosis of TLX1+ patients, already rather favourable in the LALA-94 protocol, has not been significantly improved in the paediatric-inspired GRAALL2003-2005 trial , whereas TLX3+ patients seem to have benefited particularly from the latter; the two protocols differing mainly by L-asparaginase doses. We showed that TLX1+ patients expressed less ASNS (Asparagine synthetase) than TLX3+ and TLX- patients and that this lower expression resulted from ASNS epigenetic silencing, both by methylation of the promoter and reduction of active histone marks. A low level of ASNS methylation is also associated with lower in vitro sensitivity to L-asparaginase. Finally, ASNS methylation is an independent prognostic factor for patients included in the 2003-2005 GRAALL trial suggesting that the ASNS methylation status may be relevant for the adaptation of L-asparaginase doses. In the third project, I was interested in the global DNA methylation. MeDIP-array methylation data of a series of 24 T-ALLs allowed us to identify differential methylation signatures. We then studied the methylation status in a large series of adult T-ALL by MS-MLPA using a predictor containing 9 gene promoters. We observed that main driver oncogenes dictated methylation status. TLX1+ and TLX3+ T-ALLs displayed a hypermethylated profile and conversely, SIL-TAL1+ cases were associated with a hypomethylated profile. This methylation status is also an independent prognostic factor and hypomethylated patients have a significantly unfavorable prognosis compared to hypomethylated patients. Together, these results illustrate how disruptions in epigenetic regulation can be involved both in the T-ALL oncogenesis and in the response to treatment
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Bender, Noemi [Verfasser], and Philipp [Akademischer Betreuer] Beckhove. "Molecular Mechanisms of Macrophage Activation Induced by the Synergistic Effects of Low Dose Irradiation and Adoptive T Cell Therapy / Noemi Bender ; Betreuer: Philipp Beckhove." Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180738438/34.
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Camargo, Támara Mauricio. "Economic potential of a point-of-care CD4+ T cell count diagnostic in Mexico : a case study for low-end disruption diagnostics in middle of the pyramid Latin America." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/78154.
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Thesis (S.M. in Health Sciences and Technology)--Harvard-MIT Program in Health Sciences and Technology, 2012.Cataloged from PDF version of thesis.
Includes bibliographical references (p. 92-95).
Disruptive models of innovation are starting to appear in healthcare. In the US, for instance, retail medicine clinics are changing the way in which patients satisfy their basic medical needs. In Mexico, similar retail medicine models (e.g. Farmacias Similares) are also disrupting healthcare delivery for basic medical needs. Disruptive innovations, however, are not limited to healthcare delivery, but also change the face of devices and diagnostics markets. A low CD4+ T cell count is the primary clinical indicator for HIV/AIDS disease progression, and thus is used as the primary trigger to initiate antiretroviral therapy. An entire diagnostic industry has emerged around CD4+ T cell counts for the management and treatment of HIV/AIDS patients. The diagnostic gold standards of CD4+ counts are flow cytometers. These large, capital intensive devices are commonly located in central laboratory settings, typically in urban areas. In developing nations, particularly, suburban and rural regions have no access to flow cytometers and typically face logistical problems of blood sample transportation and loss to follow-up of patients. Point-of-Care (POC) diagnostics promise disruptive models in diagnostics that will increase access, enhance care, and help better allocate healthcare resources. The concept of POC embodies the trade-off of lower "quality" (usually in the form of lower specificity and sensitivity) in exchange for higher "convenience" (i.e. better accessibility and portability, and significantly lower cost). POC diagnostics promise typical low-end and new-market disruptions in medical diagnostics and devices. Cambridge-based Daktari Diagnostics is one of such companies focused in POC diagnostics. It has developed a CD4+ T cell count diagnostic device for the management and treatment of HIV/AIDS patients. It is hypothesized in this thesis that there exists a relevant unmet medical need for POC CD4 count diagnostics in the Mexican HIV/AIDS market. In order to evaluate this hypothesis, secondary sources were reviewed, as well as primary interviews conducted across the Mexican HIV/AIDS healthcare landscape. While this hypothesis was evaluated on a preliminary basis only, responses suggested a relevant, albeit not urgent, medical need for POC CD4 count diagnostics. This primary hypothesis evaluation is extended by and complemented with market size estimations, and competitive dynamic discussions, that arrive at the following preliminary conclusions: the current market opportunity in Mexico ranges from baseline of ~100,000 tests per year to an upper bound potential of ~200,000 tests per year. In the context of this potential opportunity, Daktari's CD4 count diagnostic device is well positioned, as defined by diagnostic quality, technological characteristics, and competitive offering, to obtain a portion of this estimated market opportunity in Mexico.
by Mauricio Camargo Támara.
S.M.in Health Sciences and Technology
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Petitprez, Florent. "Integrated analysis and clinical impact of immune and stromal microenvironments in solid tumors Quantitative analyses of the tumor microenvironment composition and orientation in the era of precision medicine Transcriptomic analysis of the tumor microenvironment to guide prognosis and immunotherapies Tumor microenvironment quantification tool draws a comprehensive map of the tumor microenvironment of non-hematologic human cancers The mMCP-counter method to estimate abundance of tissue-infiltrating immune and stromal cell populations using gene expression in murine samples Immune sub-classes in sarcoma predict survival and immunotherapy response Intra-tumoral tertiary lymphoid structures are associated with a low risk of hepatocellular carcinoma early recurrence Association of IL-36γ with tertiary lymphoid structures and inflammatory immune infiltrates in human colorectal cancer Immune-based identification of cancer patients at high risk of progression Tumor-infiltrating and peripheral blood T-cell immunophenotypes predict early relapse in localized clear cell renal cell carcinoma PD-L1 expression and CD8+ T-cell infiltrate are associated with clinical progression in patients with node-positive prostate cancer Intratumoral classical complement pathway activation promotes cancer progression." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB104.
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Les tumeurs sont composées de cellules malignes et d'une grande variété de cellules non-tumorales, en particulier des cellules immunitaires qui forment le micro-environnement tumoral (MET). Il a été démontré que la composition du MET était associée au devenir clinique des patients, en termes de survie et de réponses thérapeutiques. Avec le développement récent des immunothérapies qui ciblent des éléments spécifiques du MET, l'immunité anti-tumorale a soulevé un intérêt majeur. Plusieurs méthodologies ont été mises au point afin d'étudier la composition du MET, avec une précision toujours plus grande. En particulier, des méthodes comme MCP-counter permettent d'exploiter les données transcriptomiques de la tumeur entière afin de quantifier les différentes populations qui composent le MET. Le volet méthodologique de ce travail de thèse a ainsi consisté à proposer une amélioration de MCP-counter, en particulier pour l'analyse de données RNA-Seq. Une adaptation de la méthode pour des données issues de modèles murins (mMCP-counter) est également proposée. MCP-counter permet d'analyser rapidement le MET de larges séries de tumeurs. Un second volet de cette thèse consiste en l'application de cette méthode pour établir une classification immunitaire des sarcomes des tissus mous, un type de cancer rare, hétérogène et agressif. Cette classification immunitaire a permis de mettre en évidence des groupes de tumeurs faiblement ou fortement infiltrés, ainsi qu'un groupe marqué par une forte vascularisation. De manière intéressante, la classification immunitaire permet de prédire la réponse des patients aux immunothérapies. Ce travail a aussi démontré un rôle important des structures lymphoïdes tertiaires (SLT). Les SLT sont des structures de type noeud lymphatique composées de lymphocytes B et T qui se forment dans la tumeur ou à proximité de celle-ci. Au sein des SLT, une réponse immunitaire anti-tumorale peut se former et maturer. L'intérêt porté aux SLT est de plus en plus important pour de nombreux types de cancers. Dans la plupart des types de cancer, une forte infiltration de la tumeur par des lymphocytes T, en particulier CD8+, est associée à une meilleure survie des patients. Cependant, le carcinome rénal à cellules claires et le cancer de la prostate sont des exceptions à cette règle. En effet, dans ces deux cancers urologiques, la présence dans la tumeur de lymphocytes T est associée à une survie plus courte des patients, ainsi qu'à une rechute et une progression plus précoce. Ces exceptions sont détaillées dans une troisième partie de cette thèse, par une description minutieuse du MET, ainsi que par l'analyse de l'implication du système du complément. Dans leur ensemble, les résultats présentés dans cette thèse démontrent qu'en combinant différentes méthodes d'analyse, in silico, in situ et in vivo, il est possible d'obtenir une vision extrêmement complète du MET. La connaissance des types cellulaires présents dans la tumeur ainsi que leur orientation fonctionnelle permet de guider le soin apporté aux patients et d'améliorer leur devenir clinique. La description complète du MET ouvre la voie à une médecine personnalisée pour les patients atteints de cancerTumors are composed not only of malignant cells but also contain a vast variety of non-malignant cells, notably immune cells forming the tumor microenvironment (TME). The composition of the TME was shown to be associated with clinical outcome for cancer patients, in terms of survival and therapeutic responses. With the relatively recent development of immunotherapies targeting specific elements of the TME, tumor immunology has risen a strong interest and holds a strong therapeutic potential. Several methodologies have been developed to study the composition of the TME with an increased precision. Notably, some methods such as MCP-counter enable the use of the tumor bulk transcriptome to quantify cell populations composing the TME. The methodological aspect of this PhD project consisted in setting up an enhanced version of MCP-counter that can be readily applied to RNA-Seq data, as well as propose an adaptation of the method for mouse models. Using MCP-counter, the TME of large series of tumors can be easily analyzed. The application part of this PhD work consisted of applying MCP-counter to establish an immune-based classification of soft-tissue sarcoma, a rare, aggressive and heterogeneous cancer type. The immune classification notably allowed to identify immune low and high groups, and a group characterized by a strong vasculature. Interestingly, the classification was notably found to be predictive of the patients' response to immunotherapies. It also highlighted an important role of tertiary lymphoid structures (TLS). TLS are lymph-node-like structures composed of T and B cells that form within the tumor or in close proximity. They are a site of formation and maturation of antitumoral immune responses. TLS are raising a growing interest in many malignancies. In most cancer types, a strong infiltration by T cells, in particular CD8+ T cells, is associated with a favorable clinical outcome. However, clear-cell renal cell carcinoma and prostate cancer are exceptions to this general rule. Indeed, in these urological cancers, an increased infiltration by T cells is associated with a decreased patient survival and with earlier relapse and disease progression. In a third part of this thesis, these exceptions are investigated with more details by scrutinizing the TME, and questioning the implication of the complement system. Overall, this thesis presents how the combination of several analysis methods, in silico, in situ and in vivo, can help achieve an extremely precise description of the TME. Knowing accurately what cell populations and what their functional orientation can help guide patients care and improve clinical outcome. Complete description of the TME opens the way towards personalized medicine for cancer patients
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Lin, Ming-Xian, and 林明仙. "Augmentation of T cell responses by low-affinity peptides." Thesis, 1995. http://ndltd.ncl.edu.tw/handle/60425885927638709208.
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博士國立陽明大學
微生物暨免疫學研究所
83
T細胞辨認主要組織相容性複合體(major histocompatibility complex，簡稱MHc)所呈獻的抗原胜月太。MHC與抗原胜胜月太的相互作用有如受體(receptor)與配體(ligand)一樣。胜月太可以穩定MHC的構造，以免變性及失去活性。最近的研究報告指出即使是低親合性胜月太也有穩定MHC構造的功能。在本研究裡，我們以一個對I-Ad有低親合性的胜月太PBl來探討它對抗原胜月太與I-Ad結合的影響。結果顯示PB1對I-Ad-限制型T細胞的反應有加強作用。cI 12-26變異胜月太對I-Ad-限制型及IEk-限制型T細胞的影響進一步證實了這種加強作用的可能機制。 PB1首次被發現對所有抗原專一性的I-Ad-限制型T細胞的反應都有加強作用。對I-Ad-及I-Ek-限制型T細胞的反應，或是對不經由T細胞受體(T cell receptor，TCR)辨認抗原之免疫反應，如超抗原SEB及有絲分裂原ConA，則沒有加強作用。雖然它對I-Ad只有很低的親合力，但PB1與高親合力之胜月太一樣可以穩定I-Ad的表現。此外，PBl也可增加抗原胜月太與I-Ad的結合。因此，PBl的特殊加成作用很可能是由於PBl可以穩定I-Ad的構造。而它的低親合力卻可使它易被其他高親合力的抗原胜月太取代，使抗原胜月太呈獻量增加而加強對T細胞的刺激作用。另一低親合性的胜月太TFR442-453，也藉由同樣機制而有強化T細胞反應之功能。 由上述的可能機制推測，有穩定MHC功能的低親合性胜月太就能加強其他抗原胜月太與此一MHC的結合。此一想法可由 cI 12-26變異胜月太在I-Ad的研究得到證實。用不同的cI 12-26變異胜月太做競爭結合測試，我們找到cI 12-26與I-Ad作用時所可能使用的固定殘基。雖然在固定位置做改變會顯著地降低cI 12-26與I-Ad的親合力，這些變異胜月太 (R16E,R17E及L18S)仍可以穩定I-Ad的構造，也會加強I-Ad-限制型T細胞的反應，而其他胜月太則無此功能。 我們以更進一步的實驗設計，探討cl12-26變異胜月太與 I-Ek專一性的T細胞反應的閥係，證實了此種強化機制。由於I-Ek與DR1分子有極高相似性，利用DR1的已知結構，我們成功地模擬 I-Ek的構造；並且利用競爭結合測試，確認cI 12-26與I-Ek作用的固定殘基是18S,21I,23E和26K。所有位置的變異胜月太與cI 12-26一樣可以穩定I-Ek的表現。但是只有在固定殘基做改變的變異胜月太，才能加強 I-Ek-限制型T細胞的反應。更進一步的分析顯示並非在固定殘基做改變的所有變異胜都有加強作用。類似性質的月安基酸替換(I21L,I21A,E23Y與K26R)並不會改變胜月太與I-Ek之親合力，而使這些胜月太對T細胞有競爭性的抑制作用。只有親合力顯著降低的變異胜月太(L18S,I21E,K26A,K26D及K26L)才會增加抗原胜月太與I-Ek之結合及加強T細胞之反應。 這些結果顯示了一個強化T細胞反應的新方法。低親合性胜月太可增加穩定的MHC使其兔於變性及失去活性。這些胜月太會被高親合性抗原胜月太所取代，進而增加抗原呈獻及刺激T細胞。本文的研究也說明了強化胜月太之設計可根據MHC之結合序譜而得到。在高親合性胜月太約主要固定殘基上做性質迥異的月安基酸替換，就可得到低親合性胜月太，其PBl一樣有效地加強T細胞反應。有關強化胜月太在加強免疫反應的實際運用上，正有待進一步評估。 T cells recognize antigenic peptides presented by a major histocompatibility complex (MHC). There is an intricate interplay between MHC and peptide in this ligand-receptor interaction, peptides are essential for stabilizing the MHC molecules and prevent MHC from denaturation or inactivation. Recent studies indicate that even the interaction with low-affinity peptides can stabilize MHC conformation, In this study, an I-Ad-binding peptide PBl was used to modulate the binding of antigenic peptides to I-Ad , and was found to increase T cell response restricted by I-Ad. The proposed mechanism was further confirmed by using variant peptides of cI 12-26 in both I-Ad- and I-Ek-specific T cell immunity. FBl was first found to enhance the reactivity of I-Ad restricted T cells, irrespective of the antigenic specificity. PBl had no effect on T cells specific for I-Ad and I-Ek nor did PBl increase the T cell responses to concanavalin A and staphylococcal enterotoxin B. Despite the weak affinity of PBl for I-Ad, PBl was effective as high-affinity peptide in stabilizing I-Ad expression. In addition, the binding of antigenic peptide to I-Ad was increased in the presence of PBl. Therefore, the unusual addition effect of PBl was likely due to that PBI could stabilize the I-Ad structure, and its low affinity would allow displacement by high-affinity antigenic peptides. The net result is an increased binding of antignic peptide and enhanced stimulation of T cells. A similar effect was demonstrated on a synthetic transferrin receptor peptide with minimum affinity for I-Ad. Based on the proposed mechanism, a low-peptide which retains the MHC-stabilizing ability should enhance the binding of other antigenic peptide to the given MHC. This was confirmed by using cI 12-26 with substitution at its I-Ad anchor sites. The potential I-Ad anchor sites of cl 12-26 were mapped by using competitive binding assay on site-specific mutants of cI 12-26. Despite that mutation at potential I-Ad anchor sites significantly reduced that I-Ad binding affinity, these peptides (R16E, R17E, and L18S) were able to stabilize I-Ad conformation. I-Ad-restricted T cell responses were specifically enhanced by the presence of these low-affinity peptides, but not by most other cI 12-26 variants. The augmentative mechanism was further elaborated by using cI 12-26 variants on I-Ek-specific T cells. The high homology of I-Ek with DRl enable us to simulate the structure of I-Ek based on known crystal structure of DRI. Together with competitive binding assay, the exact I-Ek anchor sites for cI 12-26 were identified as 18S, 21I, 23E, and 26K. cI 12-26 and all its site-specific mutants similarly stabilized I-EK expression, but only variant peptides with substitution at I-Ek anchor sites increased I-Ek-restricted T cell responses. Furthermore, not all mutations at anchor residues generated augmentation peptides. Substitution of anchor with a similar type of amino acid (I21L, I21A, E23A, and K26R) did not alter the I-Ek binding affinity, and the peptide competitively inhibited T cell responses. Only the mutation at anchor residues that remarkably reduced the binding affinity (L18S, 121E, K26A, K26D, and K26L) resulted in peptides which enhanced the binding of other antgenic peptides to I-Ek and increased I-Ek-specific T cell reactivity. The results support a novel approach to increase T cell immunity. Specific low-affinity peptides can be used to increase the pool of biochernically stable MHC by preventing MHC from denaturation or inactivation. The peptides can then be displaced by high-affinity antigenic peptide and resulted in enhanced antigen presentation and T cell recognition. The present study also suggest enhancing peptide can be designed according to the motif for any MHC molecule. Substitution of a major anchor site for a hgih-affinity peptide by dissimilar residues would produce peptides as effective as PBl to increase T cell response. Application of enhancing peptides in the modulation of immune response awaits further characterization.
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Lee, Chang-Dong Patrick. "Extrusion processing of low-bulk density, microcellular, open-cell thermoplastic foams." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=449923&T=F.
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Chuang, Hui-Yen, and 莊惠燕. "Serial Low-doses Sorafenib Enhance The Therapeutic Efficacy of Adoptive T cell Therapy via STAT3 Inhibition." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/43129871976029714689.
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博士國立陽明大學
生物醫學影像暨放射科學系
103
Adoptive T cells therapy (ACT) has been reported to be effective for the treatment of several types of cancers. However, ACT is not widely used in clinic mainly due to two reasons: the requirements of large numbers of transferred T cells and the hindrance of immunosuppressive tumor microenvironment. Accumulating evidences reveal that chemotherapeutic drugs could act as immune supportive rather than immunosuppressive agents when proper dosage is used, and the combination with immunotherapy often results in better outcomes than monotherapy. Immunomodulation effects of sorafenib, a multi-kinase inhibitor, have been reported in several types of cancers; however, the results are controversial at high- and low-dose. Up to present, the best dosage window of sorafenib augmenting responses of ACT while not altering host immunity is still ambiguous. Here we used a well-established E.G7/OT-1 mouse model to investigate the effects of serial low-doses of sorafenib on tumor microenvironment and therapeutic efficacy of ACT as well as the related underlying mechanisms. Sorafenib lowers the expressions of immunosuppressive factors and enhances functions and migrations of transferred cytotoxic T lymphocytes (CTLs) through inhibiting the STAT3 signaling pathway. Granzyme B promoter driven dual imaging reporters was transduced into CTLs to visualize the activation of transferred CTLs prior to ACT. Better activations of CTLs and tumor inhibitions are found in the combination group compared with both CTLs and sorafenib alone groups. Sorafenib treatment reverses the immunosuppressive microenvironment through reduction of immunosuppressive factors and immunosuppressive cells such as myeloid derived suppressive cells (MDSCs) and regulatory T cells (Tregs), and boosts the functions of transferred CTLs. These results suggest that sorafenib inhibits tumor growth not only through eradicating tumor cells but also modifying tumor microenvironment. Both contribute to the better outcomes of ACT. The findings obtained from the study may make the ACT becomes easy to apply and facilitate its progression in clinical applications.
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ALMEIDA, Afonso. "CD4+ T cell homeostasis: the thymus, the cells and the environment." Phd thesis, 2002. http://tel.archives-ouvertes.fr/tel-00002017.
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Chez les vertébrés adultes, le nombre de cellules T périphériques est soumis à un contrôle strict. Bien qu'un grand nombre de cellules T soient produites chaque jour, le nombre de cellules T à la périphérie reste constant. Chaque nouveau lymphocyte T produit ne pourra donc s'établir à la périphérie qu'après la mort d'un lymphocyte déjà établi. Dans cette optique, la sélection du répertoire des cellules T périphériques n'est pas uniquement dépendant des interactions entre une cellule et son antigène, mais elle est également dépendante d'interactions entre différentes sous-populations cellulaires (Freitas and Rocha, 2000). Dans le but de comprendre comment l'homéostasie des cellules T périphériques est atteinte, et afin de comprendre pourquoi l'homéostasie parvient à un certain niveau d'équilibre, il est important de déterminer chaque facteur intervenant dans ce processus et la contribution de chacun d'entre eux.Les cellules T sont générées dans le thymus. La production thymique de cellules T est responsable, chaque jour, de l'export de nouvelles cellules T. Cependant la taille du thymus n'est pas constante, puisque le thymus involue avec l'âge, ce qui peut avoir des conséquences sur l'homéostasie des cellules T périphériques. Il faut donc tenir compte du compartiment T central, le thymus, lorsque l'on étudie l'homéostasie des compartiments périphériques.
Le compartiment T périphérique est composé d'un certain nombre de sous-compartiments, puisque chaque cellule T n'est pas identique, et de nombreuses cellules vont se différencier à la périphérie en des sous-populations spécifiques, possédant des fonctions et des propriétés différentes. Par exemple, les sous-populations CD4+ et CD8+ devront être considérées séparément puisqu'elles sont impliquées dans différents types de réponses immunitaires et ont des mécanismes d'action différents. De la même façon, les compartiments naïfs, effecteurs et mémoires contribuent différemment à l'immuno-compétence de chaque individu. Les mécanismes impliqués dans le contrôle du nombre de chacune de ces sous-populations sont également importants pour la compréhension de l'homéostasie cellulaire T totale.
L'objectif de cette thèse a été de comprendre les mécanismes responsables de l'homéostasie périphérique T en général, et de l'homéostasie des cellules T CD4+ périphériques en particulier. Ce travail a été divisé en trois parties.
Dans la première partie de cette thèse, nous avons évalué le rôle du thymus dans la maintenance du nombre de cellules T. Nous avons développé un nouveau système expérimental nous permettant d'obtenir une estimation quantitative de la fraction des cellules précurseures pré-T compétentes, nécessaire pour assurer la fonction thymique mais aussi d'évaluer la contribution thymique à l'établissement du compartiment T périphérique. Nous avons montré qu'il n'existe pas de mécanismes homéostatiques compensatoires au cours du développement thymique. Ce résultat nous a ensuite conduit à évaluer l'effet d'un export thymique réduit sur l'établissement du compartiment T périphérique. Nous avons montré que la taille du compartiment T périphérique est indépendante du thymus, suggérant que des mécanismes compensatoires se mettent en place à la périphérie. Lorsque nous avons étudié les compartiments naïfs et activées/mémoires séparément, nous avons observé que les mécanismes compensatoires sont plus efficaces pour les sous-populations activées/mémoires.
Dans la seconde partie de cette thèse, nous avons étudié le rôle des interactions entre les cellules T périphériques dans l'établissement de l'homéostasie T périphérique. Nous avons analysé l'interaction entre les cellules T CD4+CD25+CD45RBlow (également appelées cellules T CD4+ régulatrices) et les cellules CD4+CD25-CD45RBhigh, dans des expériences de transfert chez la souris. Nous avons observé que le ratio entre les cellules CD4+CD25+CD45RBlow et les cellules CD4+CD25-CD45RBhigh transférées était déterminant pour le nombre de cellules recouvrées suggérant donc que l'interaction entre ces deux populations pourrait être déterminante pour l'homéostasie périphérique T. Nous avons testé cette hypothèse en transférant des cellules T CD4+CD25+ dans un modèle murin (les chimères de moelle osseuse CD25-/-) où l'homéostasie périphérique est perturbée et où cette sous-population CD25+ est absente. Nous avons observé que la présence de ces cellules T CD4+CD25+ dans ces chimères de moelle osseuse a pour conséquence la normalisation du compartiment T périphérique. Nous avons montré donc que l'homéostasie des cellules T périphériques est atteinte aussi grâce à la structure des sous-populations qui la constitue.
Dans la troisiéme partie de cette thèse, nous avons étudié l'importance des ressources pour la maintenance de la structure des sous-populations T périphériques. Il a été montré que le nombre de cellules T CD4+CD25+ est réduit chez les souris invalidées pour le gène de l'IL-2. Il a aussi été montré que ces souris développent des maladies auto-immunes avec des caractéristiques communes à celles développées par les souris CD25-/-. Nous avons fait l'hypothèse que le manque d'IL-2 serait responsable de la diminution de la survie des cellules T régulatrices CD4+CD25+ dans le compartiment T périphérique, et que donc les manifestations auto-immunes seraient la conséquence de la perturbation de la structure des sous-populations périphériques, puisque ces animaux ne contiennent pas cette sous-population spécifique. Nous avons testé cette hypothèse en triant les quelques cellules T CD4+CD25+ présentes chez les animaux IL2-/- et en testant leur fonction de cellules suppressives in vivo. Ces cellules ont montré leur capacité à exercer une fonction suppressive, suggérant que les souris IL-2-/- sont capable de produire des cellules régulatrices T CD4+CD25+. Nous avons confirmé ces résultats en établissant des chimères de moelle osseuse, avec des cellules provenant de la moelle osseuse d'animaux IL-2-/- et d'animaux CD25-/-. Ces animaux chimériques ne développent pas de maladies auto-immunes et le compartiment T périphérique est constitué d'une proportion normale des différentes sous-populations CD4+, notamment les CD4+CD25+. Les précurseurs issus de la moelle osseuse des animaux IL-2-/- ont donc été capables de générer une population viable de cellules T régulatrices, capable d'utiliser pour leur survie l'IL-2 produite de façon paracrine. Ces résultats illustrent bien le rôle des cytokines comme ressources majeures, notamment pour l'établissement de la structure des populations périphériques.
L'ensemble des résultats obtenus au cours de cette thèse nous a conduit à formuler que l'homéostasie des cellules T périphériques est le résultat, non seulement de l'impact thymique, mais aussi de mécanismes périphériques. Les populations sous représentées, comme la population de cellules T régulatrices CD4+CD25+, pourraient exercer un rôle important dans la maintenance de l'homéostasie des cellules T à la périphérie.
Books on the topic "Low t cell symptoms"
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W, Tsien R., Clozel Jean-Paul, and Nargeot Joël, eds. Low-voltage-activated T-type calcium channels: Proceedings from the International Electrophysiology Meeting, Montpellier, 21-22 October 1996. Chester, England: Adis International, 1998.
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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.
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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.
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Kashyap, Sangeeta. Medical Management of Endocrine Disorders after Bariatric Surgery. Edited by Tomasz Rogula, Philip Schauer, and Tammy Fouse. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190608347.003.0015.
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Endocrine complications after bariatric surgery include persistent hyperglycemia in patients with type 2 diabetes who experience initial success with weight loss. This complication occurs in those with a prolonged duration of diabetes (> 8 years) and is related to poor residual pancreatic beta-cell function. Often, weight regain is associated with recurrent diabetes, and strategies that target both weight loss and glycemic control are required. New diabetes agents, such as the SGLT2 inhibitor drug class, offer advantages to diabetes treatment after bariatric surgery. On the other end of the glycemic spectrum, hyperinsulinemic hypoglycemia occurs in patients with and without diabetes prior to surgery and often presents with little or no symptoms (i.e., neuroglycopenia). Treatment strategies involve careful monitoring of blood glucose levels and the use of low-glycemic/high-fiber diets as well as drugs that lower glucose absorption and insulin secretion. Glycemic management after bariatric surgery requires close observation.
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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Skin cancers. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0023_update_001.
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Tumours of the central nervous system examines the epidemiology, aetiology, genetics and pathology of these heterogeneous tumours. Clinical presentation reflects the site of origin and rate of growth. Investigation usually comprises imaging (MRI superior to CT for most), and biopsy; requirement for additional staging depends on pathology. The treatment of low-grade gliomas may be delayed if small with few symptoms, otherwise surgery and/or radiotherapy. High grade gliomas may be managed with surgery, radiotherapy, and temozolomide chemotherapy in fit patients. Unfit patients should be offered supportive care only. Brief summaries are provided for management of ependymoma, pineal tumours, meningioma, germ-cell CNS tumours, pituitary tumours, CNS lymphoma, acoustic neuroma, medulloblastoma, and spinal cord tumours. Radiotherapy for primary CNS tumours is described along with its side effects, and chemotherapy for these diseases is reviewed. Brain metastases far outnumber primary brain tumours, with generally poor prognosis, but this relates both to the pathology and patient performance status. Appropriate treatment may include surgery, radiotherapy, and/or chemotherapy.
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Isaacs, John D., and Philip M. Brown. Rituximab and abatacept. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083.
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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept's licence permits it use as a first-line biologic. In the United Kingdom, however, the National Institute for Health and Clinical Excellence (NICE) restricts the use of abatacept to patients who develop adverse effects with rituximab or in whom rituximab is contraindicated. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.
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Batchelor, Tracy T., Oussama Abla, Zhong-ping Chen, Dennis C. Shrieve, and Samar Issa. Tumours of the haematopoietic system. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0013.
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‘Tumours of the haematopoietic system’ examines the epidemiology, the pathogenesis, and the clinical features of adult and childhood primary central nervous system lymphomas (PCNSLs), extranodal forms of non-Hodgkin lymphoma, as well as the histiocytoses included in the World Health Organization (WHO) classification of central nervous system (CNS) tumours. It reviews these features in the most common PCNSL, primary central nervous system diffuse large B-cell lymphoma, as well as the other rare histopathological PCNSL variants including lymphomatoid granulomatosis, T-cell lymphoma, anaplastic large T-cell lymphoma, natural killer/T-cell lymphoma, low-grade lymphoma, mucosa-associated lymphoid tissue (MALT) of the dura, and Hodgkin lymphoma. The chapter also discusses clinical and anatomical PCNSL variants including vitreoretinal lymphoma, leptomeningeal lymphoma, intramedullary spinal cord lymphoma, intravascular lymphoma, and PCNSL in the immunocompromised host. It also reviews the CNS presentations of Langerhans cell histiocytosis and the following non-Langerhans cell histiocytoses: Erdheim–Chester disease, Rosai–Dorfman disease, juvenile xanthogranuloma, and histiocytic sarcoma. It is written for specialists and non-specialists managing these various conditions.
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Collins, Graham, and Chris Bunch. Lymphoma. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0289.
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Lymphoma is a cancerous disorder characterized by a clonal proliferation of lymphocytes. There are two broad categories: Hodgkin’s lymphoma, and non-Hodgkin’s lymphoma, with Hodgkin’s lymphoma defined by the presence of Reed–Sternberg cells on histological examination of affected tissue. Within the non-Hodgkin’s lymphomas, there are the much more common B-cell lymphomas and the uncommon T-cell lymphomas. Within the B-cell non-Hodgkin lymphomas, there are clinically aggressive (high-grade) forms and much more indolent (low-grade) forms. This chapter addresses the causes, diagnosis, and management of Hodgkin’s lymphoma and non-Hodgkin’s lymphoma.
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Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.
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Rush, David N., and Peter W. Nickerson. Rejection. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0283_update_001.
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Rejection of the transplanted kidney is an important cause of graft loss despite modern cross-matching techniques and immunosuppressive agents. The incidence of acute rejection episodes in the first post-transplant year is down to less than 15% in low-risk recipients, but as many as one-third of allograft losses over 10 years result from alloimmunity. Rejection may occur at any time following transplantation, from minutes—hyperacute, to days—acute, or in the longer term—chronic. Rejection can be predominantly through either T-cell-mediated or antibody-mediated mechanisms. It may present clinically as either abrupt or insidious dysfunction of the graft, or it may be subclinical and thus silent, detected only by protocol biopsy or other technology. The prevention and treatment of T-cell-mediated rejection is usually successful with current immunosuppressive agents. Antibody-mediated rejection, on the other hand, is not easily treated and is the principal cause of late renal allograft loss. This chapter presents the concepts and details of this central issue in clinical transplantation.
Book chapters on the topic "Low t cell symptoms"
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Sharma, Priyanka, and Vaibhav Neema. "Data-Aware Near Subthreshold 10 T SRAM Cell for Ultra-Low Power Application." In Lecture Notes in Electrical Engineering, 135–46. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1570-2_13.
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Christensen, Lisa Dalh, Viggo Faber, Johannes Mejer, and Per Nygaard. "Low 5′ Nucleotidase Activity in Mononuclear Cells of Patients with Defect T-Cell Function." In Advances in Experimental Medicine and Biology, 135–39. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5676-9_21.
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Fali, Tinhinane, Camille K’Ros, Victor Appay, and Delphine Sauce. "Assessing T Lymphocyte Aging Using Telomere Length and Telomerase Activity Measurements in Low Cell Numbers." In Methods in Molecular Biology, 231–43. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9728-2_18.
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Kumar, R. Manoj, and P. V. Sridevi. "Design of Look-Up Table with Low Leakage Power Enhanced Stability 10 T SRAM Cell." In Lecture Notes in Electrical Engineering, 301–14. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4058-9_27.
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Wernicke, D., M. Born, K. von der Helm, and F. Deinhardt. "Presence of Antibodies to the Human T-Cell Leukemia Virus HTLV I in German Patients with Symptoms of AIDS." In Modern Trends in Human Leukemia VI New Results in Clinical and Biological Research Including Pediatric Oncology, 338–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70385-0_71.
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Fournier, Marilaine, Mengqi Dong, and Heather J. Melichar. "Investigating T Cell Receptor Signals In Situ by Two-Photon Microscopy of Thymocytes Expressing Genetic Reporters in Low-Density Chimeras." In Methods in Molecular Biology, 221–38. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0266-9_18.
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Ferreira, Adaliene Versiani Matos, Laís Bhering Martins, Nayara Mussi Monteze, Geneviève Marcelin, and Karine Clément. "Immunology of Eating Disorders." In Immunopsychiatry, 241–50. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.003.0014.
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Eating disorders (EDs) are characterized by dysregulation in eating behavior leading to extreme increase or decrease in food intake that, in turn, changes body weight, adiposity, and physical health. Anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) are the three major eating disorders. Peculiar immune abnormalities occur in these conditions. Previous studies have reported a higher number of CD4+ T lymphocytes in patients with AN, which are related to a relative resistance to viral infections, even in the presence of leukopenia. It has also been proposed that a cluster of cytokines is altered in these patients. A chronic low-grade inflammation has been observed in obese people with BED and in patients with AN, but with a different profile in each condition. In this context, antagonist drugs of specific cytokines, such as anti-TNF, showed improvement of AN-related symptoms, but increased weight gain in obese subjects. The identification of specific molecules and/or immune cells that impair neuronal circuits implicated in eating behaviors may contribute to the development of pharmacological strategies for eating disorders.
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Kompanets, Eduard, and Viktoria Lavrynenko. "ECOSYSTEM CONNECTIONS AND FISH HEALTH." In Priority areas for development of scientific research: domestic and foreign experience. Publishing House “Baltija Publishing”, 2021. http://dx.doi.org/10.30525/978-9934-26-049-0-40.
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Ecosystems are subject to many human influences. The balance between species is disturbed due to interference with the aquatic environment. Due to environmental pollution, its impact on fish and other aquatic organisms changes. This affects ecosystem connections. Changes in the environment also change the adaptive capacity of fish, leading to impaired health. Also, there is a need to study the protective capabilities of fish from the naturally occurring opportunistic species Aeromonas hydrophila, which causes infections in them. In natural hydrobiocenoses, fish, as well as pathogens of its diseases (aeromonads) are components of food chains formed by evolution. Literature sources prove that aeromonads are normally present in microbial associations of benthic microflora as a normal saprophytic component of hydroecosystems. These bacteria feed on organic residues that are concentrated at the bottom of water bodies and perform a sanitary function, like other similar types of microorganisms. The health of fish depends on their ability to adapt to the environment. Usually in the wild, fish are rarely susceptible to disease. Local populations for a long time of coexistence have formed a certain balance with other species, including parasitic. The balance is reflected by a certain rate of abundance between species. Imbalance due to fishing from the reservoir, or, conversely, with an artificial increase in numbers, leads to changes in the aquatic environment. Changes in the habitat of fish affect themselves. Fish health is changing. In nature, such a disease as aeromonosis is an ecological concept. Violation of the ecological conditions of the species leads to stress, and reduced immunity in fish, leads to fish disease. In aeromonad infections with weak symptoms in carp, a decrease in biological parameters was observed: growth, body weight, fatness and survival (57.1%). The number of blood cells in diseased fish decreased, especially leukocytes and lymphocytes. The percentage of T- and B-lymphocytes in the blood of carp-infected carp increased. The introduction of the bacterium stimulated the immune response – an increase in the percentage of T-lymphocytes. The percentage of B cells did not increase significantly. In diseased fish, the percentage and number of low-activity T-lymphocytes increased, which corresponded to the presence of an immune response to the bacterium. The values of antibacterial activity of blood serum (BASC) in both groups of fish did not change.
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Bourke, S. J. "Pulmonary Langerhans’ cell histiocytosis." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4256–57. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0425.
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Pulmonary Langerhans’ cell histiocytosis is characterized by a reactive monoclonal proliferation of activated histiocytes in the distal bronchioles, resulting in inflammatory nodules, cyst formation, and fibrosis. Langerhans’ cells are a particular type of histiocyte derived from dendritic cells in the bone marrow. They normally migrate in the blood to the squamous epithelium of the skin, lungs, gastrointestinal, and female genital tract, where they are involved in antigen presentation to T cells. It presents with cough, breathlessness, and (sometimes) systemic symptoms. Chest radiography and CT typically show nodules which then cavitate and may rupture, causing pneumothorax. Corticosteroids and/or cytotoxic drugs are of some benefit, and lung transplantation is an option for progressive disease.
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Mukherjee, Manali, Kamarujjaman, and Mausumi Maitra. "Application of Biomedical Image Processing in Blood Cell Counting using Hough Transform." In Advanced Methods for Complex Network Analysis, 359–78. IGI Global, 2016. http://dx.doi.org/10.4018/978-1-4666-9964-9.ch015.
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In the field of biomedicine, blood cells are complex in nature. Nowadays, microscopic images are used in several laboratories for detecting cells or parasite by technician. The microscopic images of a blood stream contain RBCs, WBCs and Platelets. Blood cells are produced in the bone marrow and regularly released into circulation. Blood counts are monitored with a laboratory test called a Complete Blood Count (CBC). However, certain circumstances may cause to have fewer cells than is considered normal, a condition which is called “low blood counts”.This can be accomplished with the administration of blood cell growth factors. Common symptoms due to low red blood cells are:fatigue or tiredness, trouble breathing, rapid heart rate, difficulty staying warm, pale skin etc. Common symptoms due to low white blood cells are: infection, fever etc. It is important to monitor for low blood cell count because conditions could increase the risk of unpleasant and sometimes life-threatening side effects.
Conference papers on the topic "Low t cell symptoms"
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Sha, Wenwen, Sri Vadde, Zhili Song, Edward Seung, Zhen Xing, Liqing Chen, Virna Cortez-Retamozo, et al. "Abstract 1825: SAR443216, a novel trispecific T cell engager with potent T cell-dependent cytotoxicity for HER2-low tumors." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1825.
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Yu, Zhongnan, Yunan Zhao, Fangfang Li, Gong Chen, and Lianjun Zhang. "Sodium Butyrate Promotes CD8 T Cell Response to Low Affinity Ligand." In BIBE2020: The Fourth International Conference on Biological Information and Biomedical Engineering. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3403782.3403788.
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YASHIRO, Tsukasa. "CELL-COMPLEXES FOR t-MINIMAL SURFACE DIAGRAMS WITH 4 TRIPLE POINTS." In Intelligence of Low Dimensional Topology 2006 - The International Conference. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812770967_0047.
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Shrivastava, Prabhat Chandra, Prashant Kumar, Manish Tiwari, and Amit Dhawan. "A novel approach for Low Voltage, Low Power deep Sub-threshold 5-T SRAM cell." In 2017 International Conference on Emerging Trends in Computing and Communication Technologies (ICETCCT). IEEE, 2017. http://dx.doi.org/10.1109/icetcct.2017.8280326.
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Huang, Ya-Chi, Meng-Hsueh Chiang, Shui-Jinn Wang, and Sumeet Kumar Gupta. "An area efficient low-voltage 6-T SRAM cell using stacked silicon nanowires." In 2018 International Conference on IC Design & Technology (ICICDT). IEEE, 2018. http://dx.doi.org/10.1109/icicdt.2018.8399770.
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Ho, Chen-Ta, and Cheng-Hsien Liu. "Micro T-Switches for Cell Sorting Applications." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61427.
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A new micro-T-switch actuated by electrochemical bubbles for cells sorting has been proposed and successfully demonstrated by MEMS micromachining technique. We take advantage of electrolysis-bubbles, which have the features of low operation temperature and high surface-tension force, to actuate the micro T- switches in our device. The micro-T-switch is placed at the junction of the T-shapes microchannel. The movable T-structure design makes cell sorting active and programmable compared with other passive cell sorting mechanism such as micro-filters. Furthermore, the low operation temperature for electrolysis - bubbles driving mechanism could minimize cell-damage that happens in conventional high electric-separation instruments, such as Flow Cytometry.
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Kim, YoungBae, Qiang Tong, Ken Choi, and Yunsik Lee. "Novel 8-T CNFET SRAM cell design for the future ultra-low power microelectronics." In 2016 International SoC Design Conference (ISOCC). IEEE, 2016. http://dx.doi.org/10.1109/isocc.2016.7799768.
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Rathod, S. S., S. Dasgupta, and A. K. Saxena. "Investigation of stack as a low power design technique for 6-T SRAM cell." In TENCON 2008 - 2008 IEEE Region 10 Conference (TENCON). IEEE, 2008. http://dx.doi.org/10.1109/tencon.2008.4766757.
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Zhang, R., J. He, X. Sun, Y. Zou, Y. Gan, and Z. Li. "AB0052 Increased peripheral CD8+ T cell responses in sle by low-dose IL-2 treatment." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3196.
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Zhang, R., J. He, X. Sun, C. Li, Y. Gan, Y. Zou, and Z. Li. "357 Increased peripheral cd8 t cell responses in sle by low-dose il-2 treatment." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.357.
Full textReports on the topic "Low t cell symptoms"
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Gridley, Daila S. Mechanisms of Low Dose Radiation-induced T helper Cell Function. Office of Scientific and Technical Information (OSTI), October 2008. http://dx.doi.org/10.2172/940241.
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