Relevant bibliographies by topics / CD309

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers

Academic literature on the topic 'CD309'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "CD309"

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Meamr, Rokhsareh, Hamidreza Nikyar, Ahmad Chitsaz, Leila Dehghani, and Maryam Nasri. "Evaluation of related variables on endothelial progenitor cells in first transient ischemic attack." Journal of Shahrekord University of Medical Sciences 21, no. 4 (August 30, 2019): 157–62. http://dx.doi.org/10.34172/jsums.2019.28.

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Background and aims: In a transient ischemic attack (TIA), the activation of the endothelial progenitor cells (EPCs) has a prominent role in the formation of collateral vessels. The aim of this study was to evaluate the role of effective variables (e.g., hypertension, diabetes, hyperlipidemia, cardiovascular diseases, a family history of cardiovascular diseases, and statin therapy on the level of EPCs in TIA. Methods: Thirty patients suffering from the first attack of TIA, without having a history of acute cerebral injury, surgery or trauma, and blood disorders were enrolled in this cross-sectional study. Then, flow cytometry was utilized to estimate the level of EPCs CD34 and CD309 and the results were evaluated based on the t test or the Mann-Whitney test. Finally, the Pearson or Spearman correlation was used to establish the relationship between the variables. The level of P<0.05 was considered statistically significant in this study. Results: The mean±SD number of CD309 in patients with hyperlipidemia was less than those with no hyperlipidemia (3.35±2.77 vs. 5.59±3.85, P=0.02) and diabetic patients had a significantly higher number of CD309 compared to non-diabetics (6.14±4.89 vs, 3.5± 3.49, P=0.05). Conversely, the mean number of CD34 in groups with or without the studied variables was not statistically significant. The results further revealed that the average total of CD309 and CD34 was significantly lower in patients with hyperlipidemia as compared to those with no sign of hyperlipidemia (9.44± 3.05 vs. 6.67±4.6, P=0.02). Using logistic regression, the intended variables demonstrated no significant effects on endothelial cells, and the relationship between age and the number of progenitor cells was not significant. Conclusion: In our study, only hyperlipidemia acted as a factor influencing the numbers of EPCs. Therefore, more studies with larger sample sizes are required to discover the role of these variables on progenitor cells in TIA.
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Huang, Zhi-Xin, Jin Fang, Chang-Hua Zhou, Jie Zeng, Dong Yang, and Zhenguo Liu. "CD34+ cells and endothelial progenitor cell subpopulations are associated with cerebral small vessel disease burden." Biomarkers in Medicine 15, no. 3 (February 2021): 191–200. http://dx.doi.org/10.2217/bmm-2020-0350.

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Background: Endothelial dysfunction is considered to be involved in the pathogenesis of cerebral small vessel disease (CSVD). Endothelial progenitor cells are associated with endothelial dysfunction. The present study was designed to investigate the correlation between the populations of circulating CD34-positive cells and endothelial progenitor cells and CSVD burden. Methodology & results: A total of 364 patients with confirmed diagnosis of CSVD were included in this prospective study. Multiple ordinal logistic regression analyses showed that subjects with higher CSVD burden had significantly decreased circulating CD34+ cell level (odds ratio [OR], 0.42; p = 0.034) and significantly increased levels of circulating CD34+CD133+CD309+ and CD34+CD133+ cells (OR 1.07, p = 0.031; OR 1.03, p = 0.001, respectively), compared with patients with lower CSVD burden. Conclusion: The findings suggest that the levels of circulating CD34+ cells, CD34+CD133+CD309+ cells and CD34+CD133+ cells may be used as potential biomarkers to monitor the disease progression of CSVD.
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Younes, A., U. Consoli, V. Snell, K. Clodi, K. O. Kliche, J. L. Palmer, H. J. Gruss, et al. "CD30 ligand in lymphoma patients with CD30+ tumors." Journal of Clinical Oncology 15, no. 11 (November 1997): 3355–62. http://dx.doi.org/10.1200/jco.1997.15.11.3355.

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PURPOSE CD30 ligand (CD30L), which is expressed on resting B and activated T lymphocytes, can induce cell death in several CD30+ cell lines. Patients with CD30+ tumors (Hodgkin's disease and Ki-1+ non-Hodgkin's lymphoma) frequently have elevated soluble CD30 (sCD30) levels in their serum, which correlates with a poor prognosis. The role of sCD30 in protecting tumor cells from CD30L-mediated cell death and the pattern of CD30L expression on human peripheral-blood lymphocytes (PBLs) of normal donors and patients with CD30+ tumors are investigated. MATERIALS AND METHODS CD30L surface protein expression was determined by two-color flow cytometry on PBLs of patients with CD30+ tumors and normal individuals. CD30L levels were determined on subsets of PBLs before and after stimulation with phytohemagglutinin (PHA), anti-CD3 antibody, or CD40L. sCD30 was measured by enzyme-linked immunosorbent assay (ELISA). The apoptotic activity of membrane-bound CD30L was tested in a CD30+ cell line by the annexin V-binding method. RESULTS Unstimulated T lymphocytes of normal donors and patients with lymphoma rarely expressed CD30L surface protein, but were able to express it after stimulation with PHA or anti-CD3 antibody. Resting B cells of patients with CD30+ tumors had lower levels of detectable surface CD30L compared with normal donors (mean, 55% and 80.6%, respectively; P = .0008). Patients with high levels of serum sCD30 had lower detectable levels of CD30L on their PBLs (R2 = .72, P = .0008) and exogenous sCD30 blocked membrane-bound CD30L-mediated apoptosis in a CD30+ cell line. CONCLUSION In patients with CD30+ tumors, sCD30 can decrease the availability of CD30L on PBLs. Blocking the apoptosis-inducing activity of CD30L by its soluble receptor may explain how CD30+ tumors escape immunosurveillance and may be related to the reported poor prognosis of patients who have elevated sCD30 levels.
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Berezin, Alexander E., Alexander A. Kremzer, Daniel Petrovich, Ioana Mozos, and Alexander A. Berezin. "Association of growth-differentiation factor-15 with the number of circulating proangiogenic endothelial progenitor cells in patients with type 2 diabetes mellitus." Biomedical Research and Therapy 5, no. 7 (July 27, 2018): 2480–92. http://dx.doi.org/10.15419/bmrat.v5i7.458.

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The objective: to investigate the relationship between levels of growth differentiation factor-15 (GDF-15) and circulating number of endothelial progenitor cells (EPCs) with angiopoietin phenotypes: CD34+CD14+CD309+, and CD34+CD14+CD309+Tie2+ in patients with type 2 DM. Methods: The study was retrospectively involved 76 patients with type 2 DM aged 38 to 55 years and 30 healthy volunteers. Data collection included demographic and anthropometric information, hemodynamic performances and biomarkers of the diseases. Flow cytometry was used to determine EPCs' populations. Results: The levels of GDF-15 in peripheral blood of diabetics associated with age (r = 0.31, P = 0.044), high-sensitive C-reactive protein [hs-CRP] (r = 0.40, P = 0.001), smoking (r = 0.38, P = 0.001), body mass index [BMI] (r = 0.34, P = 0.001), LDL cholesterol (r = 0.28, P = 0.001), glycated hemoglobin [HbA1c] (r = -0.28, P = 0.001), number of CV risk factors (r = 0.26, P = 0.001). In univariate logistic regression analysis we found that level of GDF-15 ≥ 618 pg/mL, hs-CRP ≥7.12 mg/L, HbA1c ≥6.4%, fasting glucose ≥6.7 mmol/L, and BMI ≥27.3 kg/m2 predicted deficiency of both angiopoetic phenotypes of EPCs. In multivariate logistic regression model GDF-15 ≥618 pg/mL demonstrated the best odds ratio values for declining of EPCs in diabetics in comparison with other predictors including BMI, HbA1c and hs-CRP. Conclusion: GDF-15 was remarkably evaluated in type 2 DM population to healthy volunteers, and it was an independent factor that contributes to mobilization and probably proliferation of endothelial precursors with high angiopoetic activity.
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Mori, M., C. Manuelli, N. Pimpinelli, C. Mavilia, E. Maggi, M. Santucci, B. Bianchi, P. Cappugi, B. Giannotti, and M. E. Kadin. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (November 1, 1999): 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.

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Abstract Primary CD30+ cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin’s lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level. This group, which includes 2 main entities (large cell lymphoma and lymphomatoid papulosis [LyP]) and borderline cases, is characterized by the expression of CD30 antigen by neoplastic large cells at presentation, possible spontaneous regression of the skin lesions, and generally favorable clinical course. Although the functional relevance of CD30 and its natural ligand (CD30L) expression in most cases of NHL is presently undefined, previous studies indicate that CD30L is likely to mediate reduction of proliferation in CD30+ anaplastic large-cell NHL. No information is currently available concerning the expression of CD30L in primary CD30+ CTCLs. In this study, we investigated the immunophenotypic and genotypic expression of CD30 and CD30L in different developmental phases of skin lesions (growing v spontaneously regressing). By immunohistochemistry, CD30L expression was detected in regressing lesions only; by molecular analysis, the expression of CD30L was clearly higher in regressing lesions than in growing ones. CD30L, while expressed by some small lymphocytes, was most often coexpressed by CD30+neoplastic large cells, as demonstrated by 2-color immunofluorescence and by immunohistochemistry on paraffin sections. Taken together, these data suggest that CD30-CD30L interaction may play a role in the pathobiology of primary cutaneous CD30+lymphoproliferative disorders. In particular, CD30L (over)expression might have a major role in the mechanism of self-regression of skin lesions, the most distinctive clinical feature of this cutaneous lymphoma subtype.
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Mori, M., C. Manuelli, N. Pimpinelli, C. Mavilia, E. Maggi, M. Santucci, B. Bianchi, P. Cappugi, B. Giannotti, and M. E. Kadin. "CD30-CD30 Ligand Interaction in Primary Cutaneous CD30+T-Cell Lymphomas: A Clue to the Pathophysiology of Clinical Regression." Blood 94, no. 9 (November 1, 1999): 3077–83. http://dx.doi.org/10.1182/blood.v94.9.3077.421k28_3077_3083.

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Primary CD30+ cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin’s lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level. This group, which includes 2 main entities (large cell lymphoma and lymphomatoid papulosis [LyP]) and borderline cases, is characterized by the expression of CD30 antigen by neoplastic large cells at presentation, possible spontaneous regression of the skin lesions, and generally favorable clinical course. Although the functional relevance of CD30 and its natural ligand (CD30L) expression in most cases of NHL is presently undefined, previous studies indicate that CD30L is likely to mediate reduction of proliferation in CD30+ anaplastic large-cell NHL. No information is currently available concerning the expression of CD30L in primary CD30+ CTCLs. In this study, we investigated the immunophenotypic and genotypic expression of CD30 and CD30L in different developmental phases of skin lesions (growing v spontaneously regressing). By immunohistochemistry, CD30L expression was detected in regressing lesions only; by molecular analysis, the expression of CD30L was clearly higher in regressing lesions than in growing ones. CD30L, while expressed by some small lymphocytes, was most often coexpressed by CD30+neoplastic large cells, as demonstrated by 2-color immunofluorescence and by immunohistochemistry on paraffin sections. Taken together, these data suggest that CD30-CD30L interaction may play a role in the pathobiology of primary cutaneous CD30+lymphoproliferative disorders. In particular, CD30L (over)expression might have a major role in the mechanism of self-regression of skin lesions, the most distinctive clinical feature of this cutaneous lymphoma subtype.
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Barbieri, Alessandro, Marzia Dolcino, Elisa Tinazzi, Antonella Rigo, Giuseppe Argentino, Giuseppe Patuzzo, Andrea Ottria, Ruggero Beri, Antonio Puccetti, and Claudio Lunardi. "Characterization of CD30/CD30L+Cells in Peripheral Blood and Synovial Fluid of Patients with Rheumatoid Arthritis." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/729654.

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The CD30/CD30L signalling system has been implicated in the pathogenesis of several autoimmune and inflammatory conditions. In rheumatoid arthritis (RA), soluble CD30 (sCD30) levels reflect the recruitment of CD30+T cells into the inflamed joints and correlate with a positive response to immunosuppressive therapy. The aim of our report was to clarify the role of CD30/CD30L signalling system in the pathogenesis of RA. Our analysis of the CD30L+T cell subsets in peripheral blood (PB) and synovial fluid (SF) of RA patients and of the related cytokine profiles suggests the involvement of CD30/CD30L signalling in polarization of T cells towards a Th17 phenotype with proinflammatory features. Moreover, in RA SF nearly 50% of Treg cells express CD30, probably as an attempt to downmodulate the ongoing inflammation. We also show here that the engagement of CD30L on neutrophils stimulated with CD30/Fc chimera may play a crucial role in RA inflammation since activated neutrophils release IL-8, thus potentially amplifying the local inflammatory damage. In conclusion, the results obtained suggest that the complex CD30/CD30L signalling pathway is implicated in the pathogenesis and progression of RA synovitis through a concerted action on several immune effector cells.
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Ryan, Maureen, Ryan Lyski, Lauren Bou, Ryan Heiser, Bryan Grogan, Dave Meyer, Steven Jin, et al. "SGN-CD30C, an Investigational CD30-Directed Camptothecin Antibody-Drug Conjugate (ADC), Shows Strong Anti Tumor Activity and Superior Tolerability in Preclinical Studies." Blood 136, Supplement 1 (November 5, 2020): 41–42. http://dx.doi.org/10.1182/blood-2020-136577.

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SGN-CD30C, an investigational CD30-directed ADC, utilizes a potent novel camptothecin derivative as the cytotoxic payload. SGN-CD30C targets the same antigen as brentuximab vedotin (BV), though the payload has a different mechanism of action, namely inhibiting topoisomerase I rather than disrupting microtubules. Unlike monomethyl auristatin E, camptothecin-based therapies do not cause peripheral neuropathy clinically, suggesting that SGN-CD30C may have the potential to avoid one of the most common adverse events associated with BV. In preclinical studies, SGN-CD30C demonstrated strong monotherapy activity, inducing durable tumor regressions in multiple lymphoma models and eliciting cures in a BV-resistance tumor model (Figure 1). Moreover, SGN-CD30C exhibits many of the desirable attributes associated with BV, notably, bystander activity and CD30+ T regulatory cell (Treg) depletion. Using an admixed model of CD30+ and CD30-tumor cells, SGN-CD30C demonstrated robust anti-tumor activity in vivo, confirming SGN-CD30C can induce bystander killing of antigen-negative tumor cells in CD30-heterogeneous tumors. Additionally, SGN-CD30C depleted CD30+ Treg cells in vitro (Figure 2), suggesting it has the potential to exert activity through multiple mechanisms of action. SGN-CD30C was well-tolerated in non-human primate toxicology studies and demonstrated ~6-fold higher maximum tolerated dose when compared to BV. The primary toxicity for SGN-CD30C in non-human primates (NHP) studies was anemia due primarily to bone marrow suppression of erythropoiesis. SGN-CD30C had no effect on neutrophil counts and caused only minimal to mild decreases in platelets. The lack of significant neutropenia seen with SGN-CD30C contrasts with BV, indicating the two ADCs may have non-overlapping dose limiting toxicities. Hematology parameters show SGN-CD30C is tolerated at a 10-fold higher dose than BV with weekly dosing, suggesting SGN-CD30C may offer the potential for increased dose density. In summary, our data show SGN-CD30C is a compelling therapeutic candidate for CD30-positive malignancies. The distinct mechanism of action, strong anti-tumor activity, and enhanced tolerability provide a strong rationale to clinically investigate SGN-CD30C across the CD30-expressing lymphoma landscape. A Phase 1 clinical trial is planned to investigate SGN-CD30C in relapsed and refractory lymphoma. Disclosures Heiser: Seattle Genetics: Current Employment, Current equity holder in publicly-traded company. Grogan:Seattle Genetics: Current Employment, Current equity holder in publicly-traded company. Jin:Seattle Genetics: Current Employment, Current equity holder in publicly-traded company. Conerly:Seattle Genetics: Current Employment, Current equity holder in publicly-traded company.
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Bratseth, Vibeke, Hanna D. Margeirsdottir, Gemma Chiva-Blanch, Martin Heier, Svein Solheim, Harald Arnesen, Knut Dahl-Jørgensen, and Ingebjørg Seljeflot. "Annexin V+ Microvesicles in Children and Adolescents with Type 1 Diabetes: A Prospective Cohort Study." Journal of Diabetes Research 2020 (March 30, 2020): 1–8. http://dx.doi.org/10.1155/2020/7216863.

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Background. Type 1 diabetes is a chronic disease including hyperglycemia and accelerated atherosclerosis, with high risk of micro- and macrovascular complications. Circulating microvesicles (cMVs) are procoagulant cell fragments shed during activation/apoptosis and discussed to be markers of vascular dysfunction and hypercoagulability. Limited knowledge exists on hypercoagulability in young diabetics. We aimed to investigate cMVs over a five-year period in children/adolescents with type 1 diabetes compared with controls and any associations with glycemic control and cardiovascular risk factors. We hypothesized increased shedding of cMVs in type 1 diabetes in response to vascular activation. Methods. The cohort included type 1 diabetics (n=40) and healthy controls (n=40), mean age 14 years (range 11) at inclusion, randomly selected from the Norwegian Atherosclerosis and Childhood Diabetes (ACD) study. Citrated plasma was prepared and stored at -80°C until cMV analysis by flow cytometry. Results. Comparable levels of Annexin V (AV+) cMVs were observed at inclusion. At five-year follow-up, total AV+ cMVs were significantly lower in subjects with type 1 diabetes compared with controls; however, no significant differences were observed after adjusting for covariates. In the type 1 diabetes group, the total AV+, tissue factor-expressing AV+/CD142+, neutrophil-derived AV+/CD15+ and AV+/CD45+/CD15+, and endothelial-derived AV+/CD309+ and CD309+/CD34+ cMVs were inversely correlated with HbA1c (r=‐0.437, r=‐0.515, r=‐0.575, r=‐0.529, r=‐0.416, and r=‐0.445, respectively; all p≤0.01), however, only at inclusion. No significant correlations with cardiovascular risk factors were observed. Conclusions. Children/adolescents with type 1 diabetes show similar levels of AV+ cMVs as healthy controls and limited associations with glucose control. This indicates that our young diabetics on intensive insulin treatment have preserved vascular homeostasis and absence of procoagulant cMVs.
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Simhadri, Vijaya Lakshmi, Hinrich P. Hansen, Venkateswara R. Simhadri, Katrin S. Reiners, Martina Bessler, Andreas Engert, and Elke Pogge von Strandmann. "A novel role for reciprocal CD30-CD30L signaling in the cross-talk between natural killer and dendritic cells." Biological Chemistry 393, no. 1-2 (January 1, 2012): 101–6. http://dx.doi.org/10.1515/bc-2011-213.

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Abstract The interplay between dendritic cells (DCs) and natural killer (NK) cells directs adaptive immune responses. The molecular basis of the cross-talk is largely undefined. Here, we provide evidence for a contribution of CD30 (TNFRSF8) and its ligand CD30L (TNFSF8) expressed on NK cells and DCs, respectively. We demonstrate that CD30-mediated engagement of CD30L induced cytokine secretion from immature DCs via the mitogen-activated protein kinase pathway. Moreover, CD30L engagement promoted differentiation to mature DCs. On the contrary, the engagement of CD30 on NK cells resulted in an NF-κB-dependent release of TNF-α/IFN-γ. These data uncover a novel and unexpected role for CD30/CD30L that contributes to proinflammatory immune responses.
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Dissertations / Theses on the topic "CD309"

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Golbs, Sebastian. "Entzündungsparameter und Vorläufermarker bei der Coronaratherosklerose." Doctoral thesis, Universitätsbibliothek Leipzig, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:15-20100407-135735-3.

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Atherosklerotische Arterien unterliegen strukturellem Umbau und chronischer Inflammation, die von einer dynamischen Entwicklung von Vasa vasorum (VV) begleitet wird. Die Beteiligung von Leukozyten und von vaskulären Vorläuferzellen an der Neovaskularisierung sowie die intimale Hyperplasie stehen im Zentrum der Atheroskleroseforschung. Damit verbundene Erkenntnisse könnten neue therapeutische Ansätze ermöglichen. Die vorliegende Arbeit befaßt sich mit der morphologischen Verteilung von Leukozyten (CD45, CD68, Mastzellen) und von Zellen mit Vorläufermarkern (CD34, CD117, VEGFR-2) in menschlichen Coronararterien mit verschiedenen atherosklerotischen Schweregraden. Mittels immunhistologischer Technik wurden Intima und Adventitia untersucht und die Ergebnisse zu den atherosklerotischen Schweregraden und der Neovaskularisierung korreliert. In Intima, Adventitia und dem perivaskulären Fettgewebe hat die Dichte der CD45+ Lymphozyten ihr Maximum im atherosklerotischen Grad 3. Dabei konnte sowohl in der Intima als auch in der Adventitia gezeigt werden, daß eine lineare Korrelation der CD45+ Lymphozyteninfiltration und VV-Dichte vorliegt. Es wurden zwei unterschiedliche Entzündungsmuster festgestellt. Beide zeigen in Grad 3 eine Zunahme der Zelldichten. In Grad 4-5 fällt die Dichte des einen Musters (CD45+, VEGFR-2+, VV) jedoch ab, während die Dichte des anderen Musters (CD34+, CD68+, Tryptase+, CD117+) in Grad 4-5 keine Veränderung aufweist. Die Ergebnisse deuten darauf hin, daß Leukozyten und vaskuläre Vorläuferzellen im Verlauf der Atherogenese wechselnde Funktionen wahrnehmen können. Sie nehmen offensichtlich VV als Eintrittspforte in die Gefäßwand.
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Barbosa, Maria Izabel Neves de Holanda. "Avaliação do PRA e CD30s no transplante renal intervivos. Acompanhamento no 1 ano e após 6 anos em pacientes do Hospital Federal de Bonsucesso (Rio de Janeiro, Brasil)." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5592.

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O CD30 solúvel (CD30s) é uma glicoproteína transmembrana da família do fator de necrose tumoral expressa na superfície das células T. Quando este marcador é clivado ele torna-se solúvel, sendo detectado na circulação. Atualmente, o valor de CD30s pré-transplante vem sido demonstrado como um bom preditor de rejeição aguda (RA) e perda do enxerto. Poucos estudos foram realizados para sua avaliação no pós-transplante e sua correlação com sobrevida e TFG. Avaliar a eficácia da determinação dos marcadores laboratoriais CD30 solúvel (CD30s) e anticorpos reativos contra painel HLA (PRA) em seis meses, um ano e seis anos pós-transplante renal em receptores de doadores vivos, correlacionando estes marcadores com episódios de rejeição aguda, eventos infecciosos no pós-transplante, perda do enxerto e óbito do paciente transplantado. E, avaliar a correlação destes marcadores com a sobrevida do enxerto renal nestes períodos. Os pacientes estudados foram transplantados renais com doadores vivos no Hospital Federal de Bonsucesso (HFB) do Rio de Janeiro no ano de 2006 e do período de agosto de 2010 a maio de 2011, sendo uma extensão de um trabalho realizado previamente. CD30s e PRA foram analisados nas amostras coletadas no pré-transplante e com 7, 14, 21 dias, 1, 3, 6, 12 meses após o transplante e nos pacientes transplantados em 2006 amostras após 6 anos de transplante. A taxa de filtração glomerular (TFG) foi estimada utilizando MDRD e CKD-epi e 6 meses, 1 ano e 6 anos após o transplante. Os pacientes foram agrupados em 5 grupos: sem eventos, com perda do enxerto, óbito, rejeição aguda e pacientes com quadros infecciosos. Estes grupos foram avaliados com relação ao CD30s, PRA I e II e comparados dois a dois. O teste qui quadrado foi utilizado. Quando necessário aplicou-se a correção de Yates, o teste de Fisher, o teste de Kruskal-wallis. Foi considerado estatisticamente significante p<0,05. As análises foram feitas pelo programa EPI-Info (versão 3.5.3). Setenta e seis pacientes com doadores vivos foram incluídos no estudo 47 pacientes não tiveram nenhum evento (grupo 1), 7 pacientes perderam o enxerto (grupo 2), 3 pacientes faleceram (grupo 3), 11 pacientes ficaram no grupo de rejeição aguda (grupo 4) e oito pacientes tiveram infecção por CMV e herpes (grupo 5). Os pacientes do grupo de RA tiveram correlação positiva com os valores tanto de CD30s Pré-transplante (p=0,01), quanto do CD30s pós-transplante (p=0,002) e PRA I e II (p<0,001), respectivamente, quando comparados com pacientes sem eventos. A TFG tanto com MDRD e CKD-Epi não mostrou correlação com CD30s pré e pós-transplante e nem PRA I e II. A TFG com as duas fórmulas foi menor no grupo com RA comparado com o grupo sem evento após 6 anos de transplante (p=0,006). CD30s é um bom preditor de RA, assim como PRAI e II. E, também mais uma ferramenta que pode ser utilizada no acompanhamento pós-transplante Renal. A RA é um preditor isolado para diminuição de TFG no transplante.
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Fischer, Marie. "Mast cells in Hodgkin lymphoma : or 'What's a nice cell like you doing in a tumour like this?'." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4620.

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Bengtsson, Åsa. "The role of CD30 in atopic allergy /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4333-8/.

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Oberbarnscheidt, Martin. "Charakterisierung und Struktur des cd30-Gens." [S.l.] : [s.n.], 2001. http://www.diss.fu-berlin.de/2001/245/index.html.

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Hahn, Corinna. "Untersuchungen zur Apoptoseresistenz CD30-exprimierender Tumorzellen." [S.l.] : [s.n.], 2004. http://www.diss.fu-berlin.de/2004/258/index.html.

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Freitas, Helder Teixeira de. "Papel da sinalização da adenosina na geração de células T regulatórias a partir de células T naive de cordão umbilical e na imunomodulação por células-tronco estromais mesenquimais de medula óssea." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17153/tde-19072018-135504/.

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As células T regulatórias (Tregs) são essenciais para a manutenção da tolerância periférica, prevenção de doenças autoimunes e limitantes nas doenças inflamatórias crônicas. Além disso, essas células exercem um papel fundamental no controle da rejeição de transplantes. Diferentes protocolos mostraram que é possível obter Tregs a partir de células T naive CD4+ in vitro. Para tal, é consenso que o TGF-? e a interleucina-2 (IL-2) são capazes de direcionar as células T naive CD4+ a se tornarem regulatórias após um estímulo antigênico (anti-CD3/CD28). Nosso grupo recentemente notou que, durante a imunomodulação de linfócitos T pelas células estromais mesenquimais (CTMs), estas eram capazes de produzir adenosina que, por sua vez, participa do processo de imunorregulação. Outros trabalhos indicam que as CTMs suprimem a proliferação dos linfócitos T pela geração de Tregs e que as CTMs induzem a geração de Tregs através da regulação negativa da via TCR e da via AKTmTOR. Evidências apontam que a adenosina pode atuar regulando negativamente a via mTOR. Portanto, acredita-se que a adenosina possa participar do processo de geração de Tregs através da modulação da via mTOR. Além disso, estudos recentes indicam que a ativação de receptores de adenosina, mais especificamente A2a, com agentes agonistas, leva ao aumento da produção de células Tregs, enquanto que a utilização de agentes antagonistas destes receptores leva à diminuição da diferenciação de Tregs. Porém, estes estudos mostram a geração de Tregs a partir de células T naive de camundongos. Visto a grande importância das Tregs no contexto imunológico, a produção eficiente de Tregs in vitro tem importância fundamental para o desenvolvimento de novos protocolos terapêuticos para o tratamento de doenças autoimunes e no combate à rejeição de transplantes. Assim, o objetivo central deste trabalho foi avaliar a participação de agonistas e antagonistas de receptores de adenosina na indução de células T regulatórias geradas in vitro (iTreg) pela ativação de células T CD4+ naive isoladas de sangue de cordão umbilical (SCU) humano. Para isso, células mononucleares foram isoladas de bolsas de SCU e as células T naive foram isoladas imunomagnéticamente. Essas células foram ativadas com beads ligadas a anticorpos anti-CD2/CD3/CD28 e cultivadas por cinco dias na presença de IL-2 e diferentes concentrações de drogas agonistas e antagonistas de receptores de adenosina. Em seguida, foram avaliados os principais marcadores de células T regulatorias por meio de citometria de fluxo e o meio de cultura foi coletado ao final da geração para quantificação de citocinas. Além disso, o RNA total foi extraído de todas as condições de cultivo para a análise da expressão de genes envolvidos na geração e desenvolvimento das Tregs, por PCR quantitativo. O potencial de supressão de células T efetoras também foi avaliado.
Regulatory T cells (Tregs) are essential for the maintenance of peripheral tolerance, prevention of autoimmune and limiting diseases in chronic inflammatory diseases. In addition, these cells play a key role in the control of transplant rejection. Different protocols have shown that it is possible to obtain Tregs from naive CD4+ T cells in vitro. To this end, there is consensus that TGF-? and interleukin-2 (IL-2) are capable of directing the naive CD4 + T cells to become regulatory following an antigenic stimulus (anti-CD3/CD28).. Our group recently noted that during the immunomodulation of T lymphocytes by mesenchymal stromal cells (MSCs), they were able to produce adenosine which in turn participates in the immunoregulation process. Other studies indicate that MSCs suppress the proliferation of T lymphocytes by generation of Tregs and that MSCs induce generation of Tregs by downregulation of the TCR pathway and the AKT-mTOR pathway. Evidence indicates that adenosine may act by downregulating the mTOR pathway. Therefore, it is believed that adenosine may participate in the generation of Tregs by modulating the mTOR pathway. In addition, recent studies indicate that activation of adenosine receptors, more specifically A2a, with agonist agents, leads to increased production of Treg cells, whereas the use of antagonistic agents of these receptors leads to a decrease in Treg differentiation.. However, these studies show the generation of Tregs from naive T cells of mice. In view of the great importance of Tregs in the immunological context, the efficient production of Tregs in vitro is of fundamental importance for the development of new therapeutic protocols for the treatment of autoimmune diseases and in the fight against transplant rejection. Thus, the central objective of this study was to evaluate the participation of adenosine receptor agonists and antagonists in induction of regulatory T cells generated in vitro (iTreg) by the activation of naive CD4+ T cells isolated from human umbilical cord blood (SCU). For this, mononuclear cells were isolated from SCU and naive T cells were immunomagnetic isolated. These cells were activated with beads bound to anti-CD2/CD3/CD28 antibodies and cultured for five days in the presence of IL-2 and different concentrations of agonist drugs and antagonists of adenosine receptors. Next, the major regulatory T-cell markers were assessed by flow cytometry and the culture medium was collected at the end of the generation for quantification of cytokines. In addition, total RNA was extracted from all culture conditions for the analysis of the expression of genes involved in the generation and development of Tregs by quantitative PCR. The potential for suppression of effector T cells was also evaluated.
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Mac, Grogan Gaëtan. "Lymphomes cutanés à grandes cellules CD30 positives." Bordeaux 2, 1993. http://www.theses.fr/1993BOR23110.

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三井, 伸二, Masahide Takahashi, Masatoshi Ichihara, Sayaka Sobue, Kaori Ushida, Atsushi Enomoto, Masato Asai, et al. "Epidermal Hyperplasia and Appendage Abnormalities in Mice Lacking CD109." Thesis, Elsevier, 2012. http://hdl.handle.net/2237/17140.

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Brum, Liliani Mathias. "ATIVIDADE DA NTPDase DE LINFÓCITOS NA DERMATITE DE CONTATO ANTES E APÓS TRATAMENTO COM DEXAMETASONA NANOESTRUTURADA." Universidade Franciscana, 2008. http://tede.universidadefranciscana.edu.br:8080/handle/UFN-BDTD/235.

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Since the extracellular nucleotides represent an important means of modulating the activity of lymphocytes, it is essential the presence of an enzymatic mechanism to keep constant the concentration of those in the extracellular space. The activity of NTPDase has been recognized as a marker of activation necessary for the function of effector lymphocytes, participate in the processes of recognition of antigen. Contact dermatitis occurs in a delayed hypersensitivity reaction of type IV, mediated by cells through a mechanism that sensitizes the immune T lymphocyte to an antigen protein or a hapten linked to a protein. Among the mediators able to modulate the actions of lymphocytes stand out from the nucleoside and nucleotide adenine, in particular the extracellular ATP that is able to regulate the cell-cell interactions are important processes of activation, differentiation, development, proliferation, cell death and responses of effector lymphocytes. This study sought to determine first of the hydrolysis of adenine nucleotides, the NTPDase (EC 3.6.1.5, nucleoside triphosphate difosfoidrolase, CD39) in lymphocytes from mice with dermatitis induced by nickel sulphate to 5%, before and after treatment with dexamethasone and dexamethasone nanostructured free to try to check the possible changes in the activity of this enzyme front of an inflammatory reaction of type IV hypersensitivity and immunosuppressive therapy. Moreover, it was possible to verify the relationship of submission of the drug in the formulation free and nanostructures with the hydrolysis of adenine nucleotides. The average enzymatic activity of the group with contact dermatitis was significantly higher in the control group by the test of hypotheses to averages T. The results are in line with work done earlier that showed an increase of enzyme activity by the activation of lymphocytes. The hydrolysis of ATP and ADP in the group treated with dexamethasone free and in the group treated with dexamethasone nanostructured was significantly higher in the control group by analysis of variance for a way (ANOVA) followed by Kruskal-Wallis test (P < 0001). The results are in line with work done earlier that showed an increase of enzyme activity by the activation of lymphocytes. Was observed greater hydrolysis of ATP and ADP in the group treated with dexamethasone nanostructures in relation to the group treated with dexamethasone free. However, this difference was not statistically significant. Work previously shown an increase of enzyme activity during treatment with dexamethasone as a possible compensatory effect of the decrease in the number of lymphocytes. The results of this study suggest that dexamethasone nanostructures possess a immunosuppressive effects greatest, which may be the beginning of the evaluation of a more effective and safe treatment for contact dermatitis. From these results we can conclude that the determination of the activity of NTPDase in lymphocytes could be used as an indicator of the efficiency of the treatment of contact dermatitis
Uma vez que os nucleotídeos extracelulares representam uma importante via de modulação da atividade dos linfócitos, é indispensável a presença de um mecanismo enzimático capaz de manter constante a concentração desses no espaço extracelular. A atividade da NTPDase tem sido reconhecida como um marcador de ativação necessário para a função efetora dos linfócitos, participando também dos processos de reconhecimento do antígeno. Na dermatite de contato ocorre uma reação de hipersensibilidade retardada tipo IV, mediada por células, através de um mecanismo imunológico que sensibiliza os linfócitos T frente a um antígeno protéico ou a um hapteno ligado a uma proteína. Dentre os mediadores capazes de modular as ações dos linfócitos destacam-se os nucleosídeos e nucleotídeos da adenina, em especial o ATP extracelular que é capaz de regular as interações célula-célula sendo importante nos processos de ativação, diferenciação, desenvolvimento, proliferação, morte celular e respostas efetoras dos linfócitos. Este estudo procurou determinar primeiramente a hidrólise de nucleotídeos da adenina, pela NTPDase (EC 3.6.1.5, nucleosídeo trifosfato difosfoidrolase, CD39) em linfócitos de ratos com dermatite induzida por sulfato de níquel, antes e após tratamento com dexametasona livre e dexametasona nanoestruturada, para tentar verificar as possíveis alterações na atividade desta enzima frente a uma reação inflamatória de hipersensibilidade tipo IV e na terapia imunossupressora. Além disso, procurou-se verificar a possível relação da apresentação do fármaco na formulação livre e nanoestruturada com a hidrólise de nucleotídeos da adenina. A atividade enzimática média do grupo com dermatite de contato foi significativamente maior em relação ao grupo controle pelo teste de hipóteses para médias T. Os resultados encontrados estão de acordo com trabalhos realizados anteriormente que demonstram um aumento da atividade enzimática pela ativação dos linfócitos. A hidrólise do ATP e do ADP no grupo tratado com dexametasona livre e no grupo tratado com dexametasona nanoestruturada foi significativamente maior em relação ao grupo controle pelo teste de análise de variância de uma via (ANOVA) seguido pelo teste de Kruskal-Wallis (P< 0,001). Observou-se uma maior hidrólise de ADP e ATP, no grupo tratado com dexametasona nanoestruturada em relação ao grupo tratado com dexametasona livre. No entanto, esta diferença não foi estatisticamente significativa. Trabalhos anteriores já demonstraram um aumento de atividade enzimática durante tratamento com dexametasona como um possível efeito compensatório à diminuição do número de linfócitos. Os resultados deste estudo sugerem que a dexametasona nanoestruturada possui um efeito imunossupressor maior, o que pode ser o início da avaliação de um tratamento mais eficaz e seguro para a dermatite de contato. A partir destes resultados podemos concluir que a determinação da atividade da NTPDase em linfócitos poderia ser utilizada como um indicador da eficiência da terapêutica da dermatite de contato.
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Books on the topic "CD309"

1

Lin, Martin. Cloning of the human CD109 cDNA. Ottawa: National Library of Canada, 2000.

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Book chapters on the topic "CD309"

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Oflazoglu, Ezogelin, Iqbal S. Grewal, and Hanspeter Gerber. "Targeting CD30/CD30L in Oncology and Autoimmune and Inflammatory Diseases." In Advances in Experimental Medicine and Biology, 174–85. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89520-8_12.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CD39." In Encyclopedia of Signaling Molecules, 306. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100201.

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Nikolaenko, Liana, Jasmine Zain, Steven T. Rosen, and Christiane Querfeld. "CD30-Positive Lymphoproliferative Disorders." In Cancer Treatment and Research, 249–68. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99716-2_12.

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Kaczmarek, Elzbieta, Jonathan B. Siegel, Jean Sevigny, Katarzyna Koziak, Wayne W. Hancock, Adrien Beaudoin, Fritz H. Bach, and Simon C. Robson. "Vascular ATP Diphosphohydrolase (CD39/ATPDase)." In Ecto-ATPases, 171–85. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5955-9_22.

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Subtil, Antonio. "Differential Diagnosis of CD30 Expression." In Diagnosis of Cutaneous Lymphoid Infiltrates, 81–86. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11654-5_17.

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Beylot-Barry, M., and B. Vergier. "Lymphoproliférations cutanées CD30+: lymphome cutané primitif à grandes cellules T CD30+ et papulose lymphomatoïde." In Les lymphomes cutanés, 95–110. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0354-8_7.

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Kazlouskaya, V., J. Ho, and O. E. Akilov. "Case 23. Arthropod reaction with CD30 positive infiltrate and ulceration mimicking CD30 lymphoproliferative disorder." In Cutaneous Lymphomas, 50–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-59129-8_23.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Primary Cutaneous CD30-positive Lymphoproliferative Disorders." In Encyclopedia of Molecular Mechanisms of Disease, 1720. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7580.

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Kadin, Marshall E. "CD30+ Cutaneous Lymphoproliferative Disorders and Pseudolymphomas." In Cutaneous Hematopathology, 337–59. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0950-6_12.

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Kumar, Anita, Stefano Pileri, Anas Younes, and Andreas Engert. "Targeting CD30 in Patients with Hodgkin Lymphoma." In Hodgkin Lymphoma, 343–54. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12505-3_21.

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Conference papers on the topic "CD309"

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Ryan, Maureen, Ryan Lyski, Lauren Bou, David Meyer, Steven Jin, Jessica Simmons, Dennis Benjamin, Peter Senter, and Scott Jeffrey. "Abstract 2889: SGN-CD30C, a new CD30-directed camptothecin antibody-drug conjugate (ADC), shows strong anti-tumor activity and superior tolerability in preclinical studies." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2889.

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Regairaz, Anne, Caroline Laheurte, Nathalie Bonnefoy, Jean-Francois Eliaou, Gilles Alberici, Armand Bensussan, and Jeremy Bastid. "Abstract B3: CD39+ cancer cells mediate immunosuppression reverted by CD39-blocking antibodies." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-b3.

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Karkanitsa, Pavel, Sherman Weissman, Peter Rabinovich, Hinrich Abken, Andreas Hombach, Marina Komarovskaya, and Francine M. Foss. "Abstract 1936: Anti CD30 chimeric immune receptor mRNA for therapy of CD30+lymphomas." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1936.

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Savoldo, B. "CD30 CAR T for HL and ALCL." In ISCAYAHL 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1701877.

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Rana, Seema, and Rajiv Tangri. "Anaplastic large cell lymphoma ALK negative vs. peripheral T cell lymphoma (NOS) - diagnostic dilemma." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685354.

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Middle aged female presented with generalised lymphadenopathy and fever for last one month. Peripheral blood findings were within normal limits. There was no extra nodal involvement. FNAC performed initially from a cervical node suggested possibility of Hodgkin’s lymphoma and a whole node biopsy was performed. Histopathogical examination revealed effaced nodal architecture and a polymorphous population of lymphocytes, plasma cells, neutrophils and scattered large mononuclear cells with prominent nucleolus. An initial panel of CD3, CD20, LCA, CD15, CD30 and PAX5 was performed. The large atypical cells were positive for LCA, CD3 and CD30 with variable positivity for CD15. CD 30 showed Golgi and membranous staining. These large atypical cells were negative for PAX5 and CD20. In view of above findings, Hodgkin’s lymphoma was ruled out and a possibility of Non- Hodgkin’s lymphoma was considered. Further IHC markers were performed which included CD2, CD5, CD7, EMA, Alk, CD10 and KI67. CD5 showed variable positivity. The cells of interest were negative for CD2, CD7, ALK and EMA. Ki 67 index was 70-80%. Overall histological and IHC findings favoured Alk negative Anaplastic large cell lymphoma. Differential diagnosis considered was peripheral T cell lymphoma (NOS). Hodgkin’s lymphoma, peripheral T cell lymphoma (NOS) and anaplastic large cell lymphoma share common histomorphological findings. With careful analysis of Immunohistochemistry, it is easier to categorise Hodgkin’s lymphoma. ALK negative anaplastic large cell lymphoma and peripheral T cell lymphoma (NOS) are difficult to categorise and show overlapping features. We in this case have discussed clinical, histomorphological and IHC pattern of Alk negative Anaplastic large cell lymphoma.
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Heiser, Ryan A., Bryan M. Grogan, Luke S. Manlove, and Shyra J. Gardai. "Abstract 1789: CD30+T regulatory cells, but not CD30+CD8 T cells, are impaired following brentuximab vedotin treatment in vitro and in vivo." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1789.

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Gennaro, Victoria, Xiao-yong Zhang, Lauren DeSalle, Duonan Yu, Andrei Thomas-Tikhonenko, and Steven McMahon. "Abstract A40: CD30: A therapeutic target of MYC-driven cancer." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-a40.

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Bastid, Jeremy, Cécile Dejou, Jérôme Giustiniani, Stéphanie Cochaud, Gilles Alberici, Armand Bensussan, Jean-François Eliaou, and Nathalie Bonnefoy. "Abstract 5036: Blockade of the CD39 immunoregulatory pathway by monoclonal antibodies." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5036.

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Zhao, Xing, Narendiran Rajasekaran, Uwe Reusch, Jens-Peter Marschner, Martin Treder, and Holbrook E. Kohrt. "Abstract 2323: Immune checkpoint inhibition by anti-PD-1 or CD137 co-stimulation enhances cytotoxicity towards CD30+tumors mediated by the bispecific tetravalent CD30/CD16A TandAb AFM13." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2323.

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Brzoska, T., E. V. Menchikova, R. Vats, T. W. Kaminski, E. Tutuncuoglu, S. P. Tofovic, E. K. Jackson, M. T. Gladwin, and P. Sundd. "CD39 as a Master Regulator of Pulmonary Thrombosis in Sickle Cell Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7216.

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