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Letteratura scientifica selezionata sul tema "Lymphocytes"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 26 aprile 2025

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Articoli di riviste sul tema "Lymphocytes"

1

Klein, Ami, Michael Lishner, Barbara Bruser, John E. Curtis, Dominick J. Amato e Aaron Malkin. "Cortisol catabolism by lymphocytes of patients with chronic lymphocytic leukemia". Biochemistry and Cell Biology 68, n. 4 (1 aprile 1990): 810–13. http://dx.doi.org/10.1139/o90-118.

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A low rate of catabolism of cortisol by lymphocytes correlates with high sensitivity of the cells to the steroid and causes them to die at a greater rate than control samples. Since lymphocytes of patients with chronic lymphocytic leukemia respond to treatment with glucocorticosteroids and are cortisol sensitive, we attempted to see whether their capability to catabolize cortisol differs from that of normal lymphocytes. No difference was found between the two groups of cells with regard to the pattern of cortisol metabolites. However, the lymphocytes of the chronic lymphocytic leukemia groups showed a total cortisol catabolism per cell that was significantly lower than that of the control group. Patients with low lymphocyte count in peripheral blood showed a relatively higher cortisol metabolism by lymphocytes per cell than those with high counts.Key words: lymphocytes, cortisol, catabolism, chronic lymphocytic leukemia, morbidity.
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2

Spain, B. A., D. M. Soliman, R. A. Sidner e H. L. Twigg. "Enhanced proliferation and IL-2 secretion by lung lymphocytes from HIV-infected subjects". American Journal of Physiology-Lung Cellular and Molecular Physiology 269, n. 4 (1 ottobre 1995): L498—L506. http://dx.doi.org/10.1152/ajplung.1995.269.4.l498.

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Human immunodeficiency virus (HIV)-positive patients frequently develop a CD3+/CD8+ cytotoxic T cell lymphocytic alveolitis. This could occur through in situ expansion of lung lymphocytes. We evaluated lung and blood lymphocyte proliferation in asymptomatic HIV-infected individuals by measuring spontaneous and cytokine-induced tritiated thymidine incorporation. Interleukin (IL)-2 and IL-4 secretion was determined with the use of enzyme-linked immunosorbent assay, Western blotting, and immunoprecipitation techniques. Spontaneous proliferation by lung lymphocytes from HIV-positive patients was significantly greater than that of normal volunteers. Proliferation was confined to the CD8+ lymphocyte subset. Over time, spontaneous proliferation declined unless autologous alveolar macrophages (AM) were added, suggesting AM were providing additional stimulatory signals to lung lymphocytes. Lung and blood lymphocytes proliferated in response to IL-2 but not IL-4. Lymphocytes in HIV-infected lung spontaneously produced and secreted more IL-2 than either normal lung lymphocytes or autologous blood lymphocytes. IL-4 production was not detectable in either group. These findings support the hypothesis that lymphocytic alveolitis in asymptomatic HIV-positive patients results from IL-2-dependent in situ proliferation of CD3+/CD8+ cytotoxic T cells.
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3

Chen, Lin-Ying, Julia Y. S. Tsang, Yun-Bi Ni, Siu-Ki Chan, Kui-Fat Chan, Sheng Zhang e Gary M. Tse. "Lymphocyte subsets contribute to the degree of lobulitis and ductitis in sclerosing lymphocytic lobulitis of the breast". Journal of Clinical Pathology 69, n. 6 (18 novembre 2015): 527–32. http://dx.doi.org/10.1136/jclinpath-2015-203334.

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AimsSclerosing lymphocytic lobulitis (SLL) of the breast is characterised by lymphocytic lobulitis, ductitis, vasculitis and dense keloidal fibrosis with epithelioid fibroblasts. However, the subsets of the infiltrating lymphocytes and their contribution to disease progression have not been fully explored.MethodsCD20, CD3, CD4, CD8 and regulatory T (Treg) lymphocytes were evaluated in the epithelial and vascular areas in SLL. The relationship between the lymphocyte subset in different regions and the degree of inflammation was analysed.ResultsLymphocytic infiltration was mainly located in peri-lobular, peri-ductal and peri-vascular areas. No significant differences between CD20 and CD3 lymphocytes were found in peri-epithelial areas. However, there were more intra-ductal/lobular epithelial CD3 than CD20 lymphocytes (p<0.001). For T lymphocyte subsets, more CD4 than CD8 lymphocytes were found in the peri-lobular/vascular regions (p≤0.026); but an opposite trend was seen in the intra-ductal/lobular regions (p<0.001). In the peri-lobular/vascular regions, generally, different lymphocyte subsets correlated with each other. Interestingly, in the peri-ductal region, only CD4 lymphocytes showed significant correlations with all other subsets (p≤0.020). Regarding their relationship with the degree of inflammation, significant positive correlations were observed for all subsets in peri-vascular/lobular regions (p≤0.045). Only regulatory T cells, but not the others, at the peri-ductal region showed significant correlation with the degree of inflammation at all three regions (p≤0.014).ConclusionsIn addition to B lymphocyte subsets, T lymphocyte subsets could be involved differently in SLL. CD4 lymphocytes may have a pivotal role in recruiting other subsets to the inflamed site, and triggered the cascade of inflammatory changes resulting in fibrosis.
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Raje, Manoj, e Karvita B. Ahluwalia. "Motility of leukemic lymphocytes". Proceedings, annual meeting, Electron Microscopy Society of America 48, n. 3 (12 agosto 1990): 368–69. http://dx.doi.org/10.1017/s0424820100159382.

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Abstract (sommario):
In Acute Lymphocytic Leukemia motility of lymphocytes is associated with dissemination of malignancy and establishment of metastatic foci. Normal and leukemic lymphocytes in circulation reach solid tissues where due to in adequate perfusion some cells get trapped among tissue spaces. Although normal lymphocytes reenter into circulation leukemic lymphocytes are thought to remain entrapped owing to reduced mobility and form secondary metastasis. Cell surface, transmembrane interactions, cytoskeleton and level of cell differentiation are implicated in lymphocyte mobility. An attempt has been made to correlate ultrastructural information with quantitative data obtained by Laser Doppler Velocimetry (LDV). TEM of normal & leukemic lymphocytes revealed heterogeneity in cell populations ranging from well differentiated (Fig. 1) to poorly differentiated cells (Fig. 2). Unlike other cells, surface extensions in differentiated lymphocytes appear to originate by extrusion of large vesicles in to extra cellular space (Fig. 3). This results in persistent unevenness on lymphocyte surface which occurs due to a phenomenon different from that producing surface extensions in other cells.
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Hrushik, Amin, Lisa Thomas, Qi Shi, Sudeep Ruparelia, Alfonso Zangardi e Howard Nash. "Chronic Lymphocytic Leukemia with Bi-Nucleated Lymphocytes". Blood 126, n. 23 (3 dicembre 2015): 5285. http://dx.doi.org/10.1182/blood.v126.23.5285.5285.

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Abstract Introduction: B-cell chronic lymphocytic leukemia is one of the common lymphoproliferative disorders in the adult patient population. It is very uncommon to find bi-nucleated lymphocytes as a morphological feature in this disorder. Our patient was diagnosed with CLL and was found to have bi-nucleated lymphocytes in the peripheral smear. The mechanism behind this type of morphological feature of lymphocytes is unknown in CLL, and whether it has prognostic value on disease outcome is undetermined. Case Description: 62 y/o man was referred to hematology oncology after diagnosis of small cell lymphocytic leukemia was made s/p a right inguinal lymph node biopsy. His CBC revealed a wbc count of 14,000, Rbc count of 4,360, Absolute lymphocyte count of 11,500 and Platelet count of 125,000. The patient did not have any B-symptoms. On physical exam, a pertinent finding was palpable right axillary adenopathy. The CT of abdomen /pelvic to evaluate these findings. This revealed extensive axillary, abdominal/pelvic lymphadenopathy, hepatosplenomegaly and cardio phrenic lymphadenopathy. The patient had a biopsy of the right inguinal lymph node as well as bone marrow biopsy. Biopsy results showed small lymphocytic cells, some of which show occasional large nucleoli were consistent with small lymphocytic lymphoma/chronic lymphocytic leukemia, and morphologic characteristics of the lymphocytes showed bi-nucleated lymphocytes in peripheral blood smear (figure A). Flow cytometric analysis confirmed a lymphocytic population with lambda light chain restriction, expressing CD5, CD19, CD20, and CD23 consistent with chronic lymphocytic leukemia/small lymphocytic lymphoma. Bone marrow biopsy showed a hypercellular marrow with 75 % cellularity mainly composed of mature lymphocytes with scattered macrophages and eosinophils, Flow cytometric analysis (Clarient FI11-041053) of the bone marrow is interpreted as chronic lymphocytic leukemia/small cell lymphoma with the abnormal B cells representing 56% of the viable white cells. FISH study showed deletion of the ATM gene (11q22-23), D13S319 (13q14) and TP53 (p53) were observed in 29%, 71% and 35.5% of the cells analyzed, respectively. A subset of cells with the 13q deletion (20.5% of the total cells) showed homozygous deletion of D13S319 (13q14). ATM deletion is associated with progressive disease and poor prognosis in cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).He did not have any other previous history of malignancy or hematologic disorder. Discussion: B-cell chronic lymphocytic leukemia is one of the common lymphoproliferative disorders in the adult patient population. To make a diagnosis requires absolute lymphocyte count >4x10 9 and lymphoid cell morphology. In CLL, leukemic cells are small and mature appearing lymphocytes, which have regular nuclear and cytoplasmic outlines and scant weakly basophilic cytoplasm. Surface markers that define a CLL cell are proteins such as antibody light chains (kappa or lambda) and CD proteins (CD5, CD19, CD20, and CD23). In our patient absolute lymphocyte count was 11.5x109 and lymphocytic population showed surface marker lambda light chain and CD proteins CD5, CD19, CD20 and CD23 which was consistent with CLL/SLL on inguinal lymph node biopsy, but morphology of lymphocytes was small and mature bi-nucleated lymphocytes, which is very uncommon. Although bi-nucleated lymphocytes are described in a disorder "Polyclonal chronic B-cell lymphocytosis with bi-nucleated lymphocytes". Detection of an extra chromosome for the long arm of chromosome 3 +i(3)(q10) has been considered a specific marker of Polyclonal B-cell lymphocytosis with binucleated lymphocytes (PPBL),which was not present in our case. One case study by Amouroux et al, included four patients with B-cell CLL who were found to have bi-nucleated lymphocytes. Disease course was stable in one patient, one patient had an indolent course and only one required treatment due to rapid doubling time of lymphocytes. Our patient initiated chemotherapy with Rituxan and Fludara, as he had progressive disease with hepatosplenomegaly, lymph nodes and bone marrow involvement. Conclusion: Bi -nucleated lymphocytes in B-cell CLL are very rare. Explanations as to the etiology of this morphological feature in B-cell CLL is unknown. There is no sufficient evidence that bi-nucleated lymphocytes in CLL has any impact on disease progression. Disclosures No relevant conflicts of interest to declare.
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Choccalingam, Chidambharam. "Volume, conductance, and scatter parameters of neoplastic and nonneoplastic lymphocytes using Coulter LH780". Journal of Laboratory Physicians 10, n. 01 (gennaio 2018): 085–88. http://dx.doi.org/10.4103/jlp.jlp_65_17.

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Abstract PURPOSE: Automated hematology analyzers yield a complete hematological profile including a complete blood count and a differential white blood cell count. The differential count is based on analyses of three parameters, namely, volume, conductance, and scatter (VCS). We aimed to evaluate the VCS parameters, histograms, and scatterplots of neoplastic and nonneoplastic lymphocytes. MATERIAL AND METHODS: Patients were grouped into four categories, namely, acute lymphoblastic leukemia (ALL), chronic systemic disorders, chronic lymphocytic leukemia (CLL), and acute viral disease. Lymphocytes from all four groups were compared with lymphocytes from normal participants. RESULTS AND CONCLUSIONS: The histogram for acute viral disease showed a trough at T1, which was slightly obliterated, and the F1 curve mildly extended to the right. The T1 for ALL was replaced with a peak at >40% of the preset limit. The F1 peak was shifted to left for CLL. The scatterplot for viral disease showed lymphocytes extending to the variant lymphocyte window. The lymphocytes of ALL extended to the blast window, with both increase in volume and mild increase in scatter. The lymphocytes in CLL were smaller and located below the normal lymphocyte region. Mean lymphocyte volume was significantly increased in ALL and was significantly decreased in CLL. Mean lymphocyte conductance was significantly increased in CLL and significantly decreased in both acute viral disease and ALL. Mean lymphocyte scatter was significantly decreased in acute viral disease and significantly increased in ALL.
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Wiley, J. S., J. R. Chen, G. P. Jamieson e P. J. Thurlow. "Agonists for endothelial P2 purinoceptors trigger a signalling pathway producing Ca2+ responses in lymphocytes adherent to endothelial cells". Biochemical Journal 311, n. 2 (15 ottobre 1995): 589–94. http://dx.doi.org/10.1042/bj3110589.

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Recirculation of lymphocytes through the body involves their frequent adhesion to endothelial cells but little is known of the signalling pathways between these two cell types. Lymphocytes from patients with chronic lymphocytic leukaemia were loaded with the Ca(2+)-sensitive indicator, fura 2, and allowed to adhere to either glass or monolayers of human umbilical-vein endothelial cells. Addition of ATP or UTP (1-10 microM) to the superfusate produced a transient rise in cytosolic Ca2+ concentration in the lymphocytes adherent to endothelium (24 of 35 cells). In contrast, ATP or UTP (1-10 microM) had no effect on the cytosolic Ca2+ of lymphocytes attached to glass. As the only lymphocyte receptor for ATP (P2Z class) requires higher ATP concentrations (> 50 microM) for Ca2+ influx and is unresponsive to UTP, the involvement of a lymphocyte P2Z purinoceptor is unlikely. Various agonists including ATP, UTP, 2-methylthioATP, ADP and histamine all stimulated increases in endothelial cytosolic Ca2+ but only ATP and UTP (both agonists for endothelial P2U purinoceptors) triggered Ca2+ transients in adherent lymphocytes. Removal of extracellular Ca2+ did not abolish the ATP-induced rise in cytosolic Ca2+ concentration in lymphocytes adherent to endothelial cells. These findings show that stimulation of endothelial P2U purinoceptors triggers an endothelial-lymphocyte signalling pathway which releases internal Ca2+ in adherent lymphocytes.
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Winther, Birgit, Donald J. Innes, John Bratsch e Frederick G. Hayden. "Lymphocyte Subsets in the Nasal Mucosa and Peripheral Blood during Experimental Rhinovirus Infection". American Journal of Rhinology 6, n. 4 (luglio 1992): 149–56. http://dx.doi.org/10.2500/105065892781874621.

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The local cellular response during rhinovirus infection was studied with immunohistochemical staining of lymphocyte subpopulations in the lamina propria of the nasal mucosa (inferior turbinate) in 25 biopsies from volunteers with experimental rhinovirus colds and compared with biopsies from healthy volunteers. Biopsies from rhinovirus infected volunteers, taken either in the early phase of the infection (days 3 and 5) or during convalescence (day 14) were evaluated in a semiquantitative fashion for degree of infiltration. Lymphocyte subpopulations also were counted on coded specimens. During experimental rhinovirus infection, no change could be observed in the overall degree of lymphocytic infiltration or in the numbers of T and B lymphocytes compared with control specimens. The overall degree of lymphocyte infiltration in the nasal mucosa was mild to moderate and consisted principally of T lymphocytes and only a few scattered B lymphocytes. Few natural killer lymphocytes were seen. These findings are similar to those in normal nasal mucosa and in contrast to the findings after topical application of recombinant interferon, which often results in a heavy lymphocyte infiltration. Lymphocyte subpopulation in the peripheral blood did not change when compared with prechallenge values in nine rhinovirus-infected volunteers.
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Li, Lijin, Sharon M. Dial, Monika Schmelz, Margaret A. Rennels e Neil M. Ampel. "Cellular Immune Suppressor Activity Resides in Lymphocyte Cell Clusters Adjacent to Granulomata in Human Coccidioidomycosis". Infection and Immunity 73, n. 7 (luglio 2005): 3923–28. http://dx.doi.org/10.1128/iai.73.7.3923-3928.2005.

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ABSTRACT The in situ immunologic response in human coccidioidomycosis remains undefined. To explore this further, pulmonary necrotizing coccidioidal granulomata were examined using immunohistochemical staining for lymphocyte subsets and for the cytokines interleukin-10 (IL-10) and gamma interferon (IFN-γ). Discrete perigranulomatous lymphocytic clusters were seen in eight of nine tissues examined. In these tissues, T lymphocytes (CD3+) significantly outnumbered B lymphocytes (CD20+) in the mantle area of the granulomata (P = 0.028), whereas the clusters were composed of roughly equal numbers of T and B lymphocytes. While the number of cells in the mantle expressing IL-10 was similar to those in the perigranulomatous clusters, there were significantly more cells expressing IFN-γ in the mantle than in the clusters (P = 0.037). Confocal microscopy revealed that CD4+ T lymphocytes and B lymphocytes are associated with IL-10 production. CD4+CD25+ T lymphocytes were identified in the perigranulomatous clusters but were not associated with IL-10 production. This is the first report noting perigranulomatous lymphocyte clusters and IL-10 in association with human coccidioidal granulomata and suggests that down-regulation of the cellular immune response is occurring within coccidioidal granulomata.
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Zhang, Qiao-quan, Yan-fang Zhang, Nian Yu, Xing-jian Lin e Qing Di. "Differential Diagnosis of Autoimmune Encephalitis from Infectious Lymphocytic Encephalitis by Analysing the Lymphocyte Subsets of Cerebrospinal Fluid". Analytical Cellular Pathology 2019 (3 dicembre 2019): 1–6. http://dx.doi.org/10.1155/2019/9684175.

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This study is aimed at investigating the lymphocyte subsets of cerebrospinal fluid (CSF) to provide possible differential diagnostic values and better understand the pathophysiological mechanism underlying autoimmune encephalitis (AE) and infectious lymphocytic encephalitis. A series of CD markers, including CD3/4/8/20 representing different types and developmental stages of lymphocytes, were used to count the corresponding subpopulations of CSF from clinical and laboratory confirmed cases of anti-N-methyl-D-aspartate receptor AE (NMDAR-AE), herpes simplex virus encephalitis (HSVE), and tuberculous meningitis (TBM). The percentages of lymphocytes observed and the CD4 : CD8 ratios were compared between the three groups. There were no significant differences of the percentage of total lymphocytes, CD3 cells, and CD4 cells of CSF among each group. However, there were strongly statistical differences of the CD4 : CD8 ratio in CSF of each group with 0.6 : 1 in NMDAR-AE, 0.9 : 1 in HSVE, and 3.2 : 1 in TBM. The percentage of CD20 B lymphocytes in NMDAR-AE was statistically higher than that of other groups. The distinct percentages of lymphocyte subpopulations of CSF appeared to be characteristic and could potentially serve as diagnostic indicators. Further verification and research will be necessary to clarify the significance and nature of CD4 : CD8 ratios and B lymphocytes in CSF between AE and the infectious lymphocytic encephalitis.
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Tesi sul tema "Lymphocytes"

1

Culley, Donald A. "Recognition of carbohydrates by T lymphocytes in lymphocyte activation". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0022/NQ50137.pdf.

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Culley, Donald A. "Recognition of carbohyrates by T lymphocytes in lymphocyte activation". Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35686.

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The purpose of this investigation was to elucidate the role of the oligosaccharides of Class II MHC glycoproteins in allostimulation. Plasma membranes (PM) from the Daudi cell line were chemically deglycosylated using anhydrous hydrogen fluoride (HF). Subsequently, native and deglycosylated (dgl) Class II MHC molecules were affinity purified from their respective PM and inserted into the PM of peripheral blood leukocytes (PBL) which were used as stimulators in the mixed leukocyte reaction (MLR). Stimulator and responder cells were from the same donor. Both forms of the antigen were found to elicit a proliferative and cytolytic (CML) response but the dgl antigen did so to a lesser extent. Thus, it seemed as though the oligosaccharide side chains of Class II MHC molecules may not be required for allostimulation. A similar reduction in the cytolytic response was obtained when effector cells generated by the native antigen were used against targets that were stripped of N-linked oligosaccharides by tunicamycin (TM) pretreatment. Twenty-four clones were raised against the native antigen. Three clones gave proliferative responses only to the native antigen while two clones responded equally to both native and dgl antigen. In CML studies the three clones lysed normal targets but failed to lyse TM-treated target cells while the two clones did not discriminate between the two targets. Accordingly, the three clones were termed anti-MHC oligosaccharide clones while the two clones were termed anti-MHC polypeptide clones. In inhibition of CML experiments using the dgl supernatant which contained Daudi PM oligosaccharide or using a anti-MHC class II monoclonal antibody; CML reactivity of the anti-MHC oligosaccharide clones was blocked by the dgl supernatant but not by the anti-MHC MoAb. On the other hand the anti-MHC polypeptide clones were only inhibited by the anti-MHC MoAb whether against intact or TM-treated targets. These studies strongly indicate that glycoconjugates of
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3

Bonnefoy-Berard, Nathalie. "Induction et régulation de l'activation des lymphocytes T et B par les globulines antilymphocytaires". Lyon 1, 1992. http://www.theses.fr/1992LYO1H086.

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Massinga, Loembé Marguerite. "Caractérisation phénotypique et fonctionnelle des lymphocytes B dans la lymphocytose polyclonale chronique B". Thesis, Université Laval, 2004. http://www.theses.ulaval.ca/2004/22193/22193.pdf.

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La lymphocytose polyclonale chronique B (LPCB) est un syndrome peu connu caractérisé par une élévation polyclonale du nombre de lymphocytes B et de l’IgM sérique. Elle se distingue des pathologies lymphoïdes classiques par son origine polyclonale, sa grande stabilité ainsi que sa symptomatologie discrète et affecte majoritairement des femmes fumeuses. La présence de caractéristiques morphologiques et cytogénétiques distinctives, notamment cellules binucléées et anomalies génétiques (réarrangements bcl2/Ig multiples, isochromosome +i(3q)), guide le diagnostic initial. Ces particularités associées à un processus de transformation maligne contrastent avec l’apparente bénignité de la LPCB. Néanmoins, elles n’ont pas permis la délimitation précise de la population B impliquée dans la lymphocytose. Nos travaux avaient pour but d’identifier la population et les mécanismes impliqués dans l’émergence du syndrome, et éventuellement d’estimer les risques de progression clinique. En premier lieu, l’évaluation détaillée du profil immunologique des lymphocytes sanguins chez plusieurs patientes nous a permis de circonscrire formellement la lymphocytose aux cellules B IgD+IgM+CD27+. Mettant à profit les récentes avancées techniques et théoriques concernant la biologie du développement chez le lymphocyte B mature, nous avons entrepris l’analyse moléculaire des régions variables des gènes des immunoglobulines. Ces investigations ont confirmé le statut mémoire des cellules B en expansion dans la LPCB. Elles n’ont toutefois pas révélé la signature moléculaire résultant de sélection antigénique, processus central de la réponse immunitaire T-dépendante. Parallèlement, nos études fonctionnelles ont attesté de l’intégrité des molécules CD40 et AID, deux régulateurs clés de la maturation chez le lymphocyte B. Il ressort de nos analyses qu’un défaut dans la régulation de la réponse immunitaire, permettant le contournement de la sélection antigénique dans les centres germinatifs, plutôt qu’un blocage de différenciation cellulaire, serait probablement à l’origine de la lymphocytose. Alternativement, ces cellules pourraient être dérivées d’une population nouvellement caractérisée, les lymphocytes B mémoires de la zone marginale splénique, aussi retrouvés dans le sang, provenant présumement d’une voie de diversification indépendante des centres germinatifs. En conclusion, nos résultats ont permis de préciser le portrait diagnostique de la LPCB et de délimiter de nouvelles pistes de recherche touchant tant les aspects cliniques que la biologie fondamentale du syndrome.
Persistent polyclonal B cell lymphocytosis (PPBL) is an unusual haematological disorder, mainly detected in adult female smokers, that shares features of both benignity (polyclonal expansion, polyconal IgM secretion, lack of clinical symptoms, stable and mostly uneventful course); and features of malignancy (atypical binucleated cells, multiple bcl-2/Ig translocations, chromosome 3 anomalies, bone marrow involvement). Still, these morphological and clonal genetic anomalies have not been restricted to a distinctive B cell subset, and the apparent heterogeneity of the involved cellular population has long impeded further characterization of the syndrome. The aim of our research was to formally identify the population involved in the lymphocytosis, to gain some insight into the mechanisms at play in its development and to evaluate the risk for subsequent transformation in patients. Over the recent years, technical inputs from the molecular field have largely contributed to a better discrimination of the various B cells subsets and, by extension, of B cell lymphoid disorders. Thus, detailed immunophenotypic studies conducted in numerous PPBL patients allowed us to definitely circumscribe the disorder to IgD+IgM+CD27+ B lymphocytes, whereas exhaustive molecular analysis of immunoglobulin genes’ variable regions has corroborated the memory status of these cells. Yet, molecular signature of the antigenic selection process, the characteristic of a T-dependent immune response, was not detected. Sequencing of the CD40 and AID genes, key regulators in the diversification and affinity maturation of the immunoglobulin receptor, was additionally carried out and expression of both molecules was assessed. No anomaly was evidenced for either gene. In light of those observations, we conclude that a differentiation block in PPBL B lymphocytes is unlikely. Rather, we propose that defects in the affinity maturation process, namely impairment of the antigenic selection mechanism, allows the survival of low affinity IgD+IgM+CD27+ memory B lymphocytes in PPBL patients. Conversely, these cells could be related to the as yet scantily characterized IgD+IgM+CD27+ memory B cell subset from the splenic MZ, also found in the blood, and presumably derived from a germinal centre independent diversification pathway. Altogether, our results contributed to the elaboration of an accurate clinical definition for PPBL, and delineated avenues for future investigations regarding both the pathological aspects of the disorder and its purely fundamental biologic ramifications.
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De, Wit Dominique. "Tolérance immunologique induite: propriétés des lymphocytes T et des lymphocytes B". Doctoral thesis, Universite Libre de Bruxelles, 1991. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213001.

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6

Zaragoza, Bruno. "Rôle des lymphocytes T CD4+ dans l'homéostasie des lymphocytes T CD8+". Paris 6, 2009. http://www.theses.fr/2009PA066313.

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Dans une première partie, nous nous sommes concentrés sur l’homéostasie des lymphocytes T CD4+. Nous montrons que le pourcentage de cellules T CD4+CD25+ parmi les cellules T CD4+ est indexé au nombre de cellules IL-2+. Nous avons découvert que la conversion des cellules T CD4+CD25- en cellules T CD4+CD25+ était possible mais inhibé par la présence de cellules T CD4+CD25+. Enfin, dans deuxième partie, nous avons étudié le rôle des lmphocytes T CD4+ dans l’homéostasie des lymphocytes T CD8+. Le co-transfert de cellules T CD4+ naïves accroît la prolifération dûe à la lymphopénie des cellules T CD8+ augmentant de 10 à 20 fois le nombre de cellules T CD8+CD44+CD62Llow récupérées en périphérie sans modifier le nombre de cellules T CD8+CD44+CD62Lhigh. Nous montrons que l’effet auxiliaire est dépendant de l'expression de la molécule CD40 par les cellules non-B de l'hôte et de l’expression de l’IL-2 par les cellules T CD4+ naïves.
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Lumbroso, Serge. "Production spontanée in vitro par les lymphocytes circulants d'anticorps spécifiques de Brucella". Montpellier 1, 1990. http://www.theses.fr/1990MON11228.

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Rigal, Dominique. "Action de l'histamine sur la physiologie des lymphocytes : synthèse bibliographique et apport personnel". Lyon 1, 1987. http://www.theses.fr/1987LYO1H073.

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9

Turner, Lynn. "RANTES and T lymphocytes". Thesis, University of Bath, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307048.

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Björklund, Elisabet. "Multiparameter flow cytometry and minimal residual disease in patients with acute leukemia /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-624-3.

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Libri sul tema "Lymphocytes"

1

Graham, Bird Angus, e Calvert Jane E, a cura di. B lymphocytes in human disease. Oxford: Oxford University Press, 1988.

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2

Berke, Gideon, e William R. Clark. Killer Lymphocytes. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/978-1-4020-3270-7.

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Celada, Franco, e Benvenuto Pernis, a cura di. T Lymphocytes. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1.

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Berke, Gideon. Killer lymphocytes. Dordrecht: Springer, 2004.

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Immunology, British Society for, a cura di. B lymphocytes. Oxford: IRL Press at Oxford University Press, 1990.

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1938-, Clark William R., a cura di. Killer lymphocytes. Dordrecht: Springer, 2005.

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Petrov, R. V. Suppressor B lymphocytes. Chur, Switzerland: Harwood Academic Publishers, 1988.

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R, Harris James, a cura di. Lymphocytes and granulocytes. New York: Plenum Press, 1991.

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Marek, Rola-Pleszczynski, a cura di. Immunopharmacology of lymphocytes. London: Academic Press, 1994.

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Paige, Christopher J., e Roland H. Gisler, a cura di. Differentiation of B Lymphocytes. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71851-9.

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Capitoli di libri sul tema "Lymphocytes"

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Morley, J. "Lymphocytes". In Handbook of Experimental Pharmacology, 167–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73797-8_9.

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Papenfuss, Tracey, e Brad Bolon. "Lymphocytes". In Encyclopedia of Immunotoxicology, 559–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_925.

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Krüger, Karsten. "Lymphocytes". In Encyclopedia of Exercise Medicine in Health and Disease, 533–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_244.

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Romagnani, Sergio. "Lymphocytes". In Inflammatory Mechanisms in Allergic Diseases, 97–124. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9780429134432-7.

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Chinnasamy, Dhanalakashmi, e Fabio Candotti. "Lymphocytes". In Lentivirus Gene Engineering Protocols, 97–105. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1385/1-59259-393-3:97.

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Papenfuss, Tracey, e Brad Bolon. "Lymphocytes". In Encyclopedia of Immunotoxicology, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27786-3_925-2.

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Boitel, Brigitte, Myriam Ermonval, Ulrich Blank e Oreste Acuto. "T-Cell Antigen and MHC Recognition: Molecular Analysis of Human α/β TCR Specific for a Tetanus Toxin-Derived Peptide". In T Lymphocytes, 1–16. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_1.

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Hannestad, Kristian. "On the Antigenicity of Antibody Idiotypes". In T Lymphocytes, 97–104. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_10.

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Pernis, Benvenuto. "Idiotype Interactions between T Cells". In T Lymphocytes, 105–10. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_11.

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Zanetti, Maurizio. "A Network of Self Interactions". In T Lymphocytes, 111–20. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3054-1_12.

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Atti di convegni sul tema "Lymphocytes"

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Hubel, Allison, e Jeffrey McCullough. "Cryopreservation of Cultured Blood Cells for Use in Gene Therapy and Immunotherapy". In ASME 1997 International Mechanical Engineering Congress and Exposition, 97–98. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-1318.

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Abstract The freezing characteristics of genetically manipulated lymphocytes and hematopoietic stem cells were studied. The water transport characteristics of stem cells which had been cultured and transduced with a therapeutic gene were different from that of a freshly isolated cells. Changes in the freezing characteristics for genetically transformed lymphocytes were also observed. Specifically, cryopreservation protocols developed for the fresh peripheral blood lymphocytes do not produce comparable survival rates for lymphocytes which have been cultured and transduced. These results indicate that there are significant changes in the freezing characteristics resulting from the culture and transduction process.
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Pirone, Daniele, Beatrice Cavina, Martina Mugnano, Vittorio Bianco, Lisa Miccio, Anna Myriam Perrone, Anna Maria Porcelli et al. "Label-free identification of T-lymphocytes in holographic microscopy empowered by machine learning". In Digital Holography and Three-Dimensional Imaging, W4A.15. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/dh.2024.w4a.15.

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The precise count of T-lymphocytes is a challenging topic since whose number is demonstrated to correlate to disease severity. Here we report a method for label-free identification of T-lymphocytes through holographic microscopy and machine learning.
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Bruschi, Giulia, Agnese Sbrollini, Federica Pecci, Valeria Cognigni, Francesco Paoloni, Tommaso Galassi, Luca Cantini, Micaela Morettini, Rossana Berardi e Laura Burattini. "Feature Engineering Assessment of Tumor Infiltrating Lymphocytes in Lung Adenocarcinoma". In 2024 46th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC), 1–4. IEEE, 2024. https://doi.org/10.1109/embc53108.2024.10782758.

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Filippi, J. F., D. Arnoux, N. Tubiana, B. Boutière, F. Le Caär, J. Sampol, Lab Hématol, Pr J. Sampol e Pr Y. Carcassonne. "PLASMINOGEN ACTIVATOR ACTIVITY OF NORMAL AND MALIGNANT MONONUCLEAR HUMAN CELLS". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643167.

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Plasminogen activators (PA) are thought to play a role in the invasive and metastatic properties of many types of cancer cells. Though, discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells have been described.In this study, we evaluated both tissue type (tPA) and urokinase type (UK) cellular PA activities in different mononuclear cell types : normal T and B human peripheral lymphocytes, B cells from patients with chronic lymphocytic leukemia (CLL), human blood monocytes, alveolar macrophages, U 937, RAJI and JM cell 1ines.Mononuclear cells were isolated by Ficoll-hypaque gradients and monocytes by plastic adhesion. T and B cells were separated by a rosetting technique using sheep red blood cells. Cellular extracts were prepared by 0.5 % Triton X 100 buffer treatment followed by sonication and centrifugation 10 ' at 2000 g. PA assays were performed on the supernatants.UK-type PA was evaluated by a liquid-phase assay in presence of human plasminogen (Kabi) and chromogenic substrate S 2251 (Kabi).tPA was determinated using a solid-phase fibrin activity assay which involves an affinity separation step and thus allows selective detection of tPA.In both cases, results were reported in international units by reference to standard curves of UK (Choay) or tPA (Kabi).In all cell types tested, PA detected was essentially urokinase-type. Highest PA activity was found in U 937 cells (0.7 IU/5×l06 cells). In normal blood lymphocytes, mean PA activity was 0.08 IU/5×l06 cells. Examination of lymphocytes from patients with CLL revealed a marked decrease in UK activity as compared to normals (< 0.01 IU/5×106 cells in more than 50 % cases).The function of PA in normal lymphocyte physiology and the potential pathogenic role of diminished PA in CLL lymphocytes remains to be investigated.
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Aydar, S., S. Alataş, L. Numanoğlu e A. Sönmezdağ. "EFFECT OF ORAL ANTICOAGULANTS ON STABLE ROSETTE FORMATION". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643271.

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Human peripheral blood T lymphacytes when cultered in the presence of mitogen Phytohemogglutinin (PHA) acquire the capacity to form E rosettes with sheep erythrocytes that are resistant to incubation at 37° C. Whereas human thymus lymphocytes form 37° C stable E rosettes. On the other hand, it is shown that the use of anticoagulants can prevent cancer metastases which brings forth the importance of explaining the relationship between the lymphocyte functions and anticoagulant action mecha-nismus. In order to investigate this relationship, we did a group af experiments with lymphocytes of normal children and of children with severe burn wounds. Peripheral blood lymphocytes were seperated by “Lymphoprep” centrifugation technique. The lymphocytes of normal children and patients with burn were divided in two groups: A-Activated lymphocytes: 1×106 /ml lymphocytes were cultured and activated by PHAfor 48 hours at 37° C in RPMI 1640. B-Non activated lymphocytes were in culture witout PHA. 1×10™6 M/ml warfarin sulfate was added to some of the cultures of each group prior to the culture conditions. At the end of the 48 hour incubation, heat stable rosette formation was determined by the method of Wauve and co-workers. Significantly elevated levels of heat stable rosette forming cells were found in the PHA activated culture treated with warfarin sulfate in normals and patients with burn. Although the blastic transformation of T lymphocytes was found to be depressed, heat stable rosette formation of warfarin sulfate treated lymphocytes abtained from burn patients was observed to be significantly elevated. It is concluded that warfarin sulfate increases the activity of T lymphocytes by interfering with the resynthesis of heai stable E receptors.
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Al Sharifi, Liqaa, Haider Abdul Ridha, Ahmed Rashid, Sinan Muhsin e Teeb Jaafer. "Role of CD200 and CD43 in Diagnosis and Prognosis of CLL and NHL Patients". In 5th International Conference on Biomedical and Health Sciences, 317–23. Cihan University-Erbil, 2024. http://dx.doi.org/10.24086/biohs2024/paper.1403.

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Background: Chronic lymphoproliferative disorder (LPD), is a malignant disease of lymphocytes in the blood and lymphatic tissue. Chronic lymphocytic leukaemia, it is the commonest type of chronic lymphoproliferative disorder. Scoring by immunophenotyping is used to differentiate B-cell chronic lymphocytic leukemia from other B-Non-Hodgkin lymphomas. CD200 (OX2) is a glycoprotein of membrane, it is related to type I superfamily of immunoglobulin . CD43 (Sialophorin) is a sialoglycoprotein that is present on the surface of T lymphocytes, some B lymphocytes, granulocytes and monocytes, that play important role for immune function and also play a role as physiologic ligand-receptor complex involved in T- cell activation. Aim of study-Evaluate the role of CD200 and CD43 positive expression and co-expression in diagnosis and prognosis of CLL and NHL. Subjects and Methods: This cross sectional study on one hundred forty five patients with chronic lymphoprliferative disorders who were attending Baghdad teaching hospital at medical city from beginning of January 2020 to end of December 2020, patients divided in to two groups; chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma (NHL) patients At diagnosis, there was assessment of CD200 and CD43. Clinical and laboratory data were done including staging by modified Rai, and Ann arbor staging system ( for CLL and NHL respectively), then follow up for about 6-12. Results: There is significant statistical correlation between CD 200 and CD 43 and often co-expression of both in differentiation between CLL and NHL (p value < 0.001). Almost all patients of CD 200 positive expression show moderate to bright pattern of expression in CLL in apposite to NHL patients, who showed dim to moderate pattern of expression, while the great majority of CD43 expression was dim to moderate pattern in both CLL and NHL patients.In CLL patients there was no significant correlation between prognostic markers (age, Hb, platelets count, lymphocytes count and CD 38 expression) and CD200, CD 43. For NHL patients, all markers show no significant correlation except that CD 43 show significant correlation with expression of CD 38. Conclusion: CD200, CD43 and often co-expression of both have a significant value in diagnosis and differentiation of CLL from B- NHLs.
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Burmester, G., W. F. C. Rigby, E. Choy, P. Nash, K. Winthrop, P. J. Mease, P. Young et al. "SAT0330 Changes in lymphocytes and lymphocyte subsets in tofacitinib-treated patients with psoriatic arthritis". In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3490.

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Orlov, M., Z. Franklin, S. W. Wright, E. D. Morrell, M. M. Wurfel e C. Mikacenic. "CCR6+ CD4+ Lymphocytes and Innate-like Lymphocytes Are Depleted in Ventilator Associated Pneumonia". In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6611.

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Kim, Yup, Miran Lee, JooHyang Lee, Yong-Jae Lee, Sung Hoon Kim, Sang Wun Kim, Jung-Yun Lee e Junsik Park. "Peripheral lymphocytes reflect exhausted immune phenotypes of tumor-infiltrating lymphocytes in endometrial cancer patients". In The 7th Biennial Meeting of Asian Society of Gynecologic Oncology. Korea: Asian Society of Gynecologic Oncology; Korean Society of Gynecologic Oncology; Japan Society of Gynecologic Oncology, 2021. http://dx.doi.org/10.3802/jgo.2021.32.s1.omi9.

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Shawi, May, Lilian Amrein, Sergei Gryaznov, Chantal Autexier e Raquel Aloyz. "Abstract 3207: Telomerase inhibition affects fludarabine sensitivity in quiescent primary chronic lymphocytic leukemia lymphocytes". 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.am10-3207.

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Rapporti di organizzazioni sul tema "Lymphocytes"

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Avihingsanon, Yingyos, Jongkonnee Wongpiyabovorn e Nattiya Hirankarn. Biomarker discovery in systemic lupus erythematosus: genome-methylation approaches : Research report. Chulalongkorn University, 2010. https://doi.org/10.58837/chula.res.2010.15.

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Discovery of novel biomarkers in lupus nephritis Biomarkers are needed for making diagnosis and prognosis. In lupus nephritis, conventional tests like urinalysis or serum creatinine remain inadequate for patient care. In this proposal, we focused on non-invasive tools like blood and urine mRNAs or proteins. We chose candidate genes involving regulatory T-cell, B-lymphocyte signatures or vascular protective factors. Expression of regulatory cell signature (FOXP3) in peripheral blood mononuclear cells is associated with activity of lupus nephritis. We found FOXP3 mRNA levels in PBMCs from patients with active lupus nephritis were significantly lower than inactive lupus nephritis. Expression levels of FOXP3 mRNA were associated with pathological activity index, cellular crescent and fibrinoid necrosis. BLyS and APRIL are B-lymphocyte related cytokines that play an important role in generating and maintaining the mature B-cell pool. In this study, we found blood APRIL correlated with activity of lupus nephritis. Blood APRIL levels could precisely predict failure of standard treatment treatment. APRIL is a potential biomarker for predicting treatment failure. Lastly, we found an expression of VEGF in renal tissue may serve as a molecular marker of renal damage from LN and may be a predictive factor for short-term loss of kidney function in lupus nephritis patients. We proposed that reduction of intra-renal VEGF level caused by losses of podocyte cells. Genetic polymorphism of drug toxicity or pharmacokinetics in SLE patients We began to explore the pharmacokinetics and pharmacogenomics of two important immunosuppressants, azathioprine and mycophenolate. In this study, we report TPMT polymorphisms and TPMT enzyme activity were important predictors of AZA-induced myelosuppression. The tests are available for routine care. Mycophenolic acid (MPA) is active metabolite of mycophenalate. We found MPA levels is important predictor of therapeutic response. The therapeutic drug monitoring is now an important issue of patient care. We found UGT1A9 polymorphism may play a pivotal role in drug metabolisms. Methylation study We examined and compared the methylation levels of long terminal repeats (LTRs) and non-LTR retroelements in normal and SLE CD4+ T lymphocytes, CD8+ T lymphocytes and B lymphocytes. Hypomethylation of LINE-1 but not Alu was found in CD4+ T lymphocytes, CD8+ T lymphocytes, and B lymphocytes of SLE patient. Moreover, when the SLE patients were divided into active and inactive groups, LINE-1 hypomethylation was more significantly distinguished in both CD4+ and CD8+ T lymphocytes of patients from the active SLE group when compared to the controls. Genome-wide scanning using SNP microarrays In this study, we applied case-control association study including pooling genome wide association (GWA) and candidate gene association studies to search for SNPs associated with SLE susceptibility and/or severity. We could not identify any SNPs with distinct p-value or odds ratio from our pooling GWA result due to limited power. We selected IFIX for further study in candidate gene’s part. Besides IFIX, we also focus on MNDA, IFI16 and AIM2 genes which located in the same region and are all IFN-inducible genes. They are important SLE susceptibility genes due to several reasons including 1) genetic mapping from lupus murine model and 2) an upregulated IFN-inducible genes in patients with SLE from microarray studies and 3) IFI16 was identified as new autoantigen for patients with SLE. We genotyped 10 SNPs from these 4 genes and found that SNP within IFIX and IFI16 are independently important.
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Hirankarn, Nattiya, Tanapat Palaga, Yingyos Avihingsanon e Pimpayao Sodsai. The characterization of the two new genes, PTGS2 and PSN2 involving in the T lymphocyte apoptosis of lupus patients: Role of genetic polymorphism and epigenetic alteration. Chulalongkorn University, 2006. https://doi.org/10.58837/chula.res.2006.28.

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Systemic lupus erthematosus (SLE) is a prototype of autoimmune disease characterized by tissue deposition of autoantibody immune complex formation. However, etiology of disease remains unclarified. Defects of T lymphocytes lead to loss of immunological tolerance and support autoantibody production suggested that they may consistently have a central role in pathogenesis of SLE. Notch signaling is an evolutionarily conserved pathway responsible for thymocyte development, activation, proliferation, differentiation and T cell functions. Several evidences suggest Notch signaling involvement in autoimmune disorders. The aim of this study was to investigate the correlation of Notch1 receptor expression in T lymphocytes with disease progression. Twenty-two Thai SLE patients and eleven healthy controls were recruited for the study. Notch1 expression in PHA-stimulated T lymphocytes of SLE patients that indicated significantly defective regulation of Notch1 in activated T lymphocytes of SLE patients with active stage (p=0.025) while stimulated T lymphocytes of SLE patients with inactive stage were indifferent expression of Notch1 compared with healthy controls that quantified by real-time RT-PCR. It was confirmed by conventional RT-PCR that showed deceleration of Notch1 expression in SLE (p=0.015). As well as Notch1 protein expression, it was downregulated in active SLE compared to controls and inactive SLE (p=0.001 and 0.037, respectively). However, Hes1 that was target of Notch signaling did not reduce expression in SLE T lymphocytes. Moreover, proliferation capacity in SLE patients did not defect. These results showed converse correlation of Notch1 expression with severity of SLE. The data reveal the defective Notch1 in T cells that is possibly uncovered new factor of pathogenesis in SLE.
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Strube, Randall. Anti-HER2/Toxin Expressing Lymphocytes for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, maggio 2001. http://dx.doi.org/10.21236/ada395157.

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Strobe, Randall. Anti-HER2/Toxin Expressing Lymphocytes for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, maggio 2000. http://dx.doi.org/10.21236/ada393070.

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Minev, Boris R. Induction of Cytotoxic T Lymphocytes for Immunotherapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, agosto 2003. http://dx.doi.org/10.21236/ada418851.

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Palaga, Tanapat, Nattiya Hirankarn e Hathaipat Phuwapirom. Level of IL-17 in Thai SLE patients. Chulalongkorn University, 2009. https://doi.org/10.58837/chula.res.2009.30.

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Systemic Lupus Erythematosus (SLE) is an autoimmune disorder which affects various systems. Currently, the etiology of this disease has not been fully elucidated. One of potential causes which may play an important role is the defects in cytokine network and the functions of T lymphocytes. Previously, it was reported that SLE patients showed elevated elevated level of various cytokines such as IL-1β IL-6 IL-23. The aim of this study was to investigate the level of cytokine IL-17 which could be produced by various cell types including T lymphocytes CD4+ T lymphocytes mainly producing IL-17 form a distinct lineage called Th17. Differentiation of Th17 is under the influence IL-1β/IL-6 and IL-23. Furthermore, IL-23 also plays an important role in maintaining the phenotype of Th17. In this study, 29 SLE patients at King Chulalongkorn Memorial Hospital were recruited and were divided based on SLEDAI score which is an indicator of the severity of disease. There were 13 patients in active stages and 16 patients in inactive stages and 10 normal subjects were used as control group. First, the frequency of T lymphocytes expressing IL-23R in PBMC was analyzed. The frequency of CD4+IL-23R+ and CD8+IL-23R+T lymphocytes in PBMC from SLE patients were found to be significantly higher than those of controls, both in freshly isolated PBMC (day 0) (p=0.0025, p=0.0201 and p=0.0021 for CD4+ and p=0.0021, p=0.0032 and p=0.0008 for CD8+ for the inactive, the active and the total SLE groups in comparison with normal subjects, respectively) and PBMC receiving ex vivo stimulation by anti-CD3 and CD28 antibodies (day 3) (p=0.0057, p=0.0011 and p=0.0007 for CD4+ and p=0.0041, p=0.0101 and p=0.0019 for CD8+ for the inactive, the active and the total SLE groups in comparison with normal subjects, respectively). When the frequency of T cells which could produce IL-17 was measured, PBMC from SLE patients showed significantly lower percentages of CD4+IL-17+ T lymphocytes than those from the control group in samples from day 0 (p=0.0219 and p = 0.0197 for the inactive and the total SLE in comparison with normal subjects, respectively) but the trend reversed on day 3 when SLE patients exhibited a tendency to have higher percentage of CD4+IL-17+ T cells. In contrast, the frequency of CD8+IL-17+T cells in SLE patients was significantly higher on day 3 (p=0.0007, p=0.0007, p=0.0120 and p=0.0007 for the inactive, the active and the total SLE in comparison with normal subjects, respectively), while there was no difference on day 0. When the level of IL-17 in serum and plasma were measured by ELISA, only two samples were found to show detectable IL-17 at 5.12-6.78 pg/ml, while the level in the rest of the samples was below detectable. When IL-23 was measured in sera by ELISA, all samples showed negative results. Therefore, the expression of IL-17A was analyzed by Realtime RT-PCR and it was found that PBMC from patients showed increased, but not statistically significant, level of IL-17A, when compared with the controls. Analysis of all results obtained in this study, the correlation was found to be significant between percentages of CD4+IL-23R+, CD8+IL-23R+T lymphocytes and CD4+IL-17+, CD8+IL-17+ T lymphocytes in SLE patients. Furthermore, the percentages of CD4+IL-23R+T cells at day 3 were found to have a correlation with IL-17A expression in SLE patients. When the active patients were compared against the inactive patients for all indicators investigated in this study, no statistically significant difference was detected. Taken together, these results suggest that T lymphocytes in SLE patients increase IL-23R and IL-17 expression, which may play an important role in pathology of SLE.
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Albertini, R. J. The development of in vitro mutagenicity testing systems using t-lymphocytes. Office of Scientific and Technical Information (OSTI), febbraio 1998. http://dx.doi.org/10.2172/615639.

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Albertini, R. J. The development of in vitro mutagenicity testing systems using T-lymphocytes. Office of Scientific and Technical Information (OSTI), maggio 1992. http://dx.doi.org/10.2172/7049865.

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Mekova, Ralitsa V., Spaska S. Lesichkova, Adelina D. Tsakova, Julieta Z. Bakalova, Deniz Bakalov e Mihail Boyanov. Circulating CD3(+)CD4(+)CD28(‒) T Lymphocytes in Patients with Autoimmune Thyroiditis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, maggio 2020. http://dx.doi.org/10.7546/crabs.2020.05.14.

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Beuneu, Helene, Sandra Demaria e Michael Dustin. Visualizing Breast Cancer Cell Interaction with Tumor-Infiltrating Lymphocytes During Immunotherapy. Fort Belvoir, VA: Defense Technical Information Center, aprile 2013. http://dx.doi.org/10.21236/ada577265.

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