Thematische Bibliographien / CD44 B-Lymphocytes Lymphocyte Activation

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Auswahl der wissenschaftlichen Literatur zum Thema „CD44 B-Lymphocytes Lymphocyte Activation“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 13. Februar 2022

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Zeitschriftenartikel zum Thema "CD44 B-Lymphocytes Lymphocyte Activation"

Rivière, Elodie, Juliette Pascaud, Nicolas Tchitchek, Saida Boudaoud, Audrey Paoletti, Bineta Ly, Anastasia Dupré et al. „Salivary gland epithelial cells from patients with Sjögren’s syndrome induce B-lymphocyte survival and activation“. Annals of the Rheumatic Diseases 79, Nr. 11 (25.08.2020): 1468–77. http://dx.doi.org/10.1136/annrheumdis-2019-216588.

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ObjectivePrimary Sjögren's syndrome (pSS) is characterised by chronic hyperactivation of B lymphocytes. Salivary gland epithelial cells (SGECs) could play a role in promoting B-lymphocyte activation within the target tissue. We aimed to study the interactions between SGECs from patients with pSS or controls and B lymphocytes.MethodsPatients had pSS according to 2016 European League Against Rheumatism/American College of Rheumatology criteria. Gene expression analysis of SGECs and B lymphocytes from pSS and controls isolated from salivary gland biopsies and blood was performed by RNA-seq. SGECs from pSS and controls were cocultured with B-lymphocytes sorted from healthy donor blood and were stimulated. Transwell and inhibition experiments were performed.ResultsGene expression analysis of SGECs identified an upregulation of interferon signalling pathway and genes involved in immune responses (HLA-DRA, IL-7 and B-cell activating factor receptor) in pSS. Activation genes CD40 and CD48 were upregulated in salivary gland sorted B lymphocytes from patients with pSS. SGECs induced an increase in B-lymphocyte survival, which was higher for SGECs from patients with pSS than controls. Moreover, when stimulated with poly(I:C), SGECs from patients with pSS induced higher activation of B-lymphocytes than those from controls. This effect depended on soluble factors. Inhibition with anti-B-cell activating factor, anti-A proliferation-inducing ligand, anti-interleukin-6-R antibodies, JAK1/3 inhibitor or hydroxychloroquine had no effect, conversely to leflunomide, Bruton's tyrosine kinase (BTK) or phosphatidyl-inositol 3-kinase (PI3K) inhibitors.ConclusionsSGECs from patients with pSS had better ability than those from controls to induce survival and activation of B lymphocytes. Targeting a single cytokine did not inhibit this effect, whereas leflunomide, BTK or PI3K inhibitors partially decreased B-lymphocyte viability in this model. This gives indications for future therapeutic options in pSS.

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Ilangumaran, Subburaj, Anne Briol und Daniel C. Hoessli. „CD44 Selectively Associates With Active Src Family Protein Tyrosine Kinases Lck and Fyn in Glycosphingolipid-Rich Plasma Membrane Domains of Human Peripheral Blood Lymphocytes“. Blood 91, Nr. 10 (15.05.1998): 3901–8. http://dx.doi.org/10.1182/blood.v91.10.3901.

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Abstract CD44 is the major cell surface receptor for the extracellular matrix glycosaminoglycan hyaluronan and is implicated in a variety of biological events that include embryonic morphogenesis, lymphocyte recirculation, inflammation, and tumor metastasis. CD44 delivers activation signals to T lymphocytes, B lymphocytes, natural killer cells, polymorphonuclear leukocytes, and macrophages by stimulating protein tyrosine phosphorylation and calcium influx. The mechanism of signal transduction via CD44 remains undefined, although CD44 was shown to physically associate with intracellular protein tyrosine kinase Lck in T lymphocytes. In the present report, we show that a significant proportion of CD44 in human peripheral blood T lymphocytes and endothelial cells is associated with low-density plasma membrane fractions that represent specialized plasma membrane domains enriched in glycosphingolipids and glycosylphosphatidylinositol (GPI)-anchored proteins. CD44 and the GPI-anchored CD59 do not appear to directly interact in the low-density membrane fractions. In human peripheral blood T lymphocytes, 20% to 30% of the Src family protein tyrosine kinases, Lck and Fyn, are recovered from these fractions. CD44-associated protein kinase activity was selectively recovered from the low-density membrane fractions, corresponding to glycosphingolipid-rich plasma membrane microdomains. Reprecipitation of the in vitro phosphorylated proteins showed that CD44 associates not only with Lck but also with Fyn kinase in these membrane domains. Our results suggest that cellular stimulation via CD44 may proceed through the signaling machinery of glycosphingolipid-enriched plasma membrane microdomains and, hence, depend on the functional integrity of such domains.

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CD44 is the major cell surface receptor for the extracellular matrix glycosaminoglycan hyaluronan and is implicated in a variety of biological events that include embryonic morphogenesis, lymphocyte recirculation, inflammation, and tumor metastasis. CD44 delivers activation signals to T lymphocytes, B lymphocytes, natural killer cells, polymorphonuclear leukocytes, and macrophages by stimulating protein tyrosine phosphorylation and calcium influx. The mechanism of signal transduction via CD44 remains undefined, although CD44 was shown to physically associate with intracellular protein tyrosine kinase Lck in T lymphocytes. In the present report, we show that a significant proportion of CD44 in human peripheral blood T lymphocytes and endothelial cells is associated with low-density plasma membrane fractions that represent specialized plasma membrane domains enriched in glycosphingolipids and glycosylphosphatidylinositol (GPI)-anchored proteins. CD44 and the GPI-anchored CD59 do not appear to directly interact in the low-density membrane fractions. In human peripheral blood T lymphocytes, 20% to 30% of the Src family protein tyrosine kinases, Lck and Fyn, are recovered from these fractions. CD44-associated protein kinase activity was selectively recovered from the low-density membrane fractions, corresponding to glycosphingolipid-rich plasma membrane microdomains. Reprecipitation of the in vitro phosphorylated proteins showed that CD44 associates not only with Lck but also with Fyn kinase in these membrane domains. Our results suggest that cellular stimulation via CD44 may proceed through the signaling machinery of glycosphingolipid-enriched plasma membrane microdomains and, hence, depend on the functional integrity of such domains.

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Shimonaka, Mika, Koko Katagiri, Toshinori Nakayama, Naoya Fujita, Takashi Tsuruo, Osamu Yoshie und Tatsuo Kinashi. „Rap1 translates chemokine signals to integrin activation, cell polarization, and motility across vascular endothelium under flow“. Journal of Cell Biology 161, Nr. 2 (21.04.2003): 417–27. http://dx.doi.org/10.1083/jcb.200301133.

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Chemokines arrest circulating lymphocytes within the vasculature through the rapid up-regulation of leukocyte integrin adhesive activity, promoting subsequent lymphocyte transmigration. However, the key regulatory molecules regulating this process have remained elusive. Here, we demonstrate that Rap1 plays a pivotal role in chemokine-induced integrin activation and migration. Rap1 was activated by secondary lymphoid tissue chemokine (SLC; CCL21) and stromal-derived factor 1 (CXCL4) treatment in lymphocytes within seconds. Inhibition of Rap1 by Spa1, a Rap1-specific GTPase-activating protein, abrogated chemokine-stimulated lymphocyte rapid adhesion to endothelial cells under flow via intercellular adhesion molecule 1. Expression of a dominant active Rap1V12 in lymphocytes stimulated shear-resistant adhesion, robust cell migration on immobilized intercellular adhesion molecule 1 and vascular cell adhesion molecule 1, and transendothelial migration under flow. We also demonstrated that Rap1V12 expression in lymphocytes induced a polarized morphology, accompanied by the redistribution of CXCR4 and CD44 to the leading edge and uropod, respectively. Spa1 effectively suppressed this polarization after SLC treatment. This unique characteristic of Rap1 may control chemokine-induced lymphocyte extravasation.

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Mun, Yeung-Chul, Kyoung-Eun Lee, Jung Mi Kwon, Seung-Hyun Nam, Eun Sun Yoo, Yun-Kyung Bae, Seung-Eun Lee et al. „Establishment of Effective B Lymphocyte Ex Vivo Expansion on Human Cord Blood Using TPO, SCF, FL, IL-4, IL-10, and CD40L.“ Blood 104, Nr. 11 (16.11.2004): 2882. http://dx.doi.org/10.1182/blood.v104.11.2882.2882.

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Abstract In respect to B lymphocyte-mediated immunity, characteristics of human cord blood are low counts of mature B lymphocytes, deficient expression of CD40L and cytokine production in CD4+ T lymphocytes, defect in the isotype switch of immunoglobulin and the activation of B lymphocytes, and low IgG production of B lymphocytes. These characteristics of the B lymphocyte from human cord blood lead to a delayed B lymphocyte-mediated immune reconstitution and an increased susceptibility to infections after a cord blood transplantation. The mechanism of immunological recostitution after cord blood transplantation has been examined from a variety of viewpoints in experimental models as well as clinical studies. However, problems of sustained immunodeficiency after cord blood transplantation remain to be resolved. The aim of the present study is to establish culture conditions that support the effective B lymphocyte expansion of human cord blood using IL-4, IL-10, and CD40L, to which cytokines are defected in B lymphocyte of human cord blood, and established conditions are compared to previously established cytokine combinations, TPO+SCF+FL in our Lab (Br J Haematol 107:176–185, 1999 & Stem Cells 21:228–235, 2003). To elucidate the effective B lymphocyte-mediated immune reconstitution of cord blood after ex vivo expansion, mononuclear cells, separated from density gradient of Ficoll system, and CD34+ purified cells, isolated from immunomicrobead(MiniMACS) system, were cultured with various combinations of cytokines (TPO+FL+SCF and/or IL-4, IL-10 and CD40L) for 2 weeks or 4 weeks. This then allowed for cytometric analysis after immunofluorescence stain with CD34, CD38 (for HSC analysis) and CD19, IgG and IgM (for B lymphocyte-mediated immune reconstitution) and CD4 (for T helper cell) and CD25 (for lymphocyte activation assay) to be performed. In the B lymphocyte expansion aspect, the immunoglobulin expression, and functional activity, expansion with the TPO+FL+SCF+IL-4+IL-10 combination showed best results in the expression of CD19, CD25, IgG, and IgM. However, the addition of CD40L to those culture condition did not increase expression of CD19, CD25, IgG, and IgM after the expansion of human cord blood. Expansion of CD34+ purified cells was superior to MNCs in the expression of CD19, CD25, IgG, and IgM. In consideration for the duration of cultures, the 2 week culture was superior to the 4 week culture with respect to graft stemness (CD34+CD38- fraction). Our data suggests most superior results were observed from the ex vivo expansion of CD34+ purified cells cultured for 2 weeks with TPO+FL+SCF+IL-4+IL-10, in the B lymphocyte-mediated immune reconstitution and graft stemness aspect. The results of this study warrant further investigation on effective B lymphocyte-mediated immune reconstitution after cord blood transplantation in vivo using ex vivo expanded cord blood.

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Zhang, Jinyi, Amro Shehabeldin, Luis A. G. da Cruz, Jeffrey Butler, Ally-Khan Somani, Mary McGavin, Ivona Kozieradzki et al. „Antigen Receptor–Induced Activation and Cytoskeletal Rearrangement Are Impaired in Wiskott-Aldrich Syndrome Protein–Deficient Lymphocytes“. Journal of Experimental Medicine 190, Nr. 9 (01.11.1999): 1329–42. http://dx.doi.org/10.1084/jem.190.9.1329.

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The Wiskott-Aldrich syndrome protein (WASp) has been implicated in modulation of lymphocyte activation and cytoskeletal reorganization. To address the mechanisms whereby WASp subserves such functions, we have examined WASp roles in lymphocyte development and activation using mice carrying a WAS null allele (WAS−/−). Enumeration of hemopoietic cells in these animals revealed total numbers of thymocytes, peripheral B and T lymphocytes, and platelets to be significantly diminished relative to wild-type mice. In the thymus, this abnormality was associated with impaired progression from the CD44−CD25+ to the CD44−CD25− stage of differentiation. WASp-deficient thymocytes and T cells also exhibited impaired proliferation and interleukin (IL)-2 production in response to T cell antigen receptor (TCR) stimulation, but proliferated normally in response to phorbol ester/ionomycin. This defect in TCR signaling was associated with a reduction in TCR-evoked upregulation of the early activation marker CD69 and in TCR-triggered apoptosis. While induction of TCR-ζ, ZAP70, and total protein tyrosine phosphorylation as well as mitogen-activated protein kinase (MAPK) and stress-activated protein/c-Jun NH2-terminal kinase (SAPK/JNK) activation appeared normal in TCR-stimulated WAS−/− cells, TCR-evoked increases in intracellular calcium concentration were decreased in WASp-deficient relative to wild-type cells. WAS−/− lymphocytes also manifested a marked reduction in actin polymerization and both antigen receptor capping and endocytosis after TCR stimulation, whereas WAS−/− neutrophils exhibited reduced phagocytic activity. Together, these results provide evidence of roles for WASp in driving lymphocyte development, as well as in the translation of antigen receptor stimulation to proliferative or apoptotic responses, cytokine production, and cytoskeletal rearrangement. The data also reveal a role for WASp in modulating endocytosis and phagocytosis and, accordingly, suggest that the immune deficit conferred by WASp deficiency reflects the disruption of a broad range of cellular behaviors.

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Zöller, M. „CD44, metastatic tumor spread, lymphocyte activation“. Biomedicine & Pharmacotherapy 47, Nr. 4 (Januar 1993): 174. http://dx.doi.org/10.1016/0753-3322(93)90013-b.

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Maltzman, J. S., J. A. Carman und J. G. Monroe. „Role of EGR1 in regulation of stimulus-dependent CD44 transcription in B lymphocytes.“ Molecular and Cellular Biology 16, Nr. 5 (Mai 1996): 2283–94. http://dx.doi.org/10.1128/mcb.16.5.2283.

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The immediate-early gene egr-1 encodes a transcription factor (EGR1) that links B-cell antigen receptor (BCR) signals to downstream activation events through the regulation of previously unidentified target genes. Here we identify the gene encoding the lymphocyte homing and migration protein CD44 as a target of EGR1 regulation in B cells. BCR-induced increases in CD44 mRNA expression and transcription levels are shown to occur in EGR1-expressing but not in nonexpressing subclones of the B-cell line WEHI-231. Kinetics of egr-1 transcription and the appearance of nuclear EGR1 protein precede CD44 induction and occur within 30 min after stimulation in the EGR1-expressing subclone. A single EGR1 binding motif is demonstrated at bp -301 of the human CD44 promoter. Cotransfection of a CD44 promoter-chloramphenicol acetyltransferase reporter construct with an egr-1 expression vector resulted in a 6.5- to 8.5-fold induction of transcriptional activity relative to an empty expression vector. The EGR1 binding motif was shown to be necessary for stimulus-induced expression of a CD44 promoter-chloramphenicol acetyltransferase reporter construct in nontransformed B lymphocytes and was required for transactivation by an EGR1 expression vector in a B-cell line. These studies identify EGR1 as an intermediary linking BCR-derived signals to the induction of CD44. The relevance of these molecular events to BCR signal transduction and antigen-stimulated B-cell-mediated immune responses is discussed.

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Forster, R., T. Emrich, E. Kremmer und M. Lipp. „Expression of the G-protein--coupled receptor BLR1 defines mature, recirculating B cells and a subset of T-helper memory cells“. Blood 84, Nr. 3 (01.08.1994): 830–40. http://dx.doi.org/10.1182/blood.v84.3.830.bloodjournal843830.

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The G-protein-coupled receptor BLR1 related to receptors for chemokines and neuropeptides has been identified as the first lymphocyte-specific member of the gene family characterized by seven transmembrane-spanning regions. Using a high-affinity anti-BLR1 monoclonal antibody (MoAb) and three-color flow cytometry it is shown that BLR1 expression on peripheral blood cells is limited to B cells and to a subset of CD4+ (14%) and CD8+ (2%) lymphocytes. T cells expressing BLR1 were positive for CD45R0, were negative for interleukin-2 receptors, show high levels of CD44, and show low levels of L-selectin. The majority of CD4+ cells originating from secondary lymphatic tissue, but none of cord blood- derived T cells, express BLR1. These observations suggest that BLR1 is a marker for memory T cells. Furthermore, BLR1 expression was detected on all CD19+ peripheral or tonsillar B lymphocytes, but only on a fraction of cord blood cells and bone marrow cells expressing CD19, sIgM, or sIgD. Interestingly, activation of both mature B and T cells by CD40 MoAb and CD3 MoAb, respectively, led to complete downregulation of BLR1. These data suggest that the G-protein-coupled receptor BLR1 is involved in functional control of mature recirculating B cells and T- helper memory cells participating in cell migration and cell activation.

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Murakami, S., und H. Okada. „Lymphocyte-Fibroblast Interactions“. Critical Reviews in Oral Biology & Medicine 8, Nr. 1 (Januar 1997): 40–50. http://dx.doi.org/10.1177/10454411970080010201.

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Chronic inflammatory reactions are usually characterized by inflammatory cell accumulation in the extravascular connective tissue. In such sites, inappropriate activation of circulating or resident lymphocytes becomes self-perpetuating and can lead to chronic tissue destruction. In addition to that, the locally infiltrated lymphocytes should have an opportunity to interact directly with fibroblasts composing the connective tissue. The direct interactions of those different cell types seem to play important roles in lymphocyte lodging and retention in such sites. Thus, for clarification of the immunopathogenesis of the chronic inflammatory diseases, including periodontitis, it is important that the molecular mechanisms involved in the heterotypic cell-cell interactions be revealed. In fact, it has been demonstrated that lymphocytes interact with various non-hematopoietic cells, such as epithelial cells and endothelial cells. Regarding interactions with fibroblasts, it has been shown that IFNγ-stimulated fibroblasts can regulate the proliferative responses of T-lymphocytes both positively and negatively. Furthermore, activated lymphocytes have demonstrated strong binding ability to various fibroblast cell lines. Blocking experiments utilizing monoclonal antibodies specific to various cell adhesion molecules revealed that very late antigen (VLA) integrins, lymphocyte-function-associated antigen (LFA-1)/intercellular adhesion molecule-1 (ICAM-1), CD44/hyarulonate are, at least in part, involved in lymphocyte-fibroblast interactions. In addition, recent findings raised the possibility that the adhesive interactions between lymphocytes and fibroblasts influenced the various cellular functions of each cell type. In fact, it was recently demonstrated that the adhesive interactions stimulated fibroblasts to increase expression of inflammatory cytokine mRNA. These results strongly suggest that fibroblasts are not merely innocent bystanders but actively participate in local inflammatory reactions by directly interacting with locally infiltrated lymphocytes.

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Mehr Quellen

Dissertationen zum Thema "CD44 B-Lymphocytes Lymphocyte Activation"

Wyant, Tiana L. „Influence of Anti-CD44 on Murine B Cell Activation“. VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/1004.

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Lymphocyte activation and trafficking are indispensable to the immune system. CD44, an adhesion molecule, plays important roles in T cell activation, lymphocyte homing/trafficking, and tumor metastasis. Although the functions of CD44 have been shown in T cells and other leukocytes, little is known about its role in B cells. The effects of CD44 cross-linking on murine B cell activation via CD40L/IL-4 was explored using the anti-CD44 mAbs RK3G9 and IM7. Immobilized RK3G9 and IM7 could strongly inhibit B cell proliferation and Ig production, with IgE inhibition being prominent. Soluble anti-CD44 had no effect. The inhibitory effect of RK3G9 was not influenced by addition of anti-FCγRII, indicating no role for the inhibitory receptor. The effects of delayed addition of immobilized anti-CD44 mAbs were studied, and the results indicated no inhibition after 96 hrs of culture. B cells were also activated by either LPS or anti-IgM F(ab')2. While LPS-induced B cell activation was inhibited by immobilized anti-CD44 mAbs, anti-IgM activation was refractory. Interestingly, addition of both anti-IgM and CD40L or LPS resulted in some modulation of the inhibitory activity. Additionally, FACS and Elispot revealed that RK3G9-treated cells had reduced numbers of plasma cells. Taken together, these results suggest that CD44 cross-linking could control polyclonal B cell activation by CD40L, but allow sIgM/CD40L activation to continue.

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Fournier-Conge, Anne-Marie. „Anomalies de l'activation des lymphocytes B circulants au cours de l'infection par le VIH-1 : implications physiopathologiques et cliniques“. Montpellier 1, 1996. http://www.theses.fr/1996MON1T025.

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DiSanto, James Philip. „Molecular events in human T cell activation : CD4, CD8 and the human Lyt-3 molecules /“. Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=745024391&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Sutherland, Claire Louise. „Structure/function analysis of CD40, a key activator of B lymphocytes“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0027/NQ38986.pdf.

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Delli, Joe. „Coreceptor and costimulatory signals organize proteins within the immunological synapse and augment proximal T cell signaling events /“. Connect to full text via ProQuest. IP filtered, 2006.

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Thesis (Ph.D. in Immunology) -- University of Colorado, 2006.
Typescript. Includes bibliographical references (leaves 277-285). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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Hermann, Patrice. „Recherche du ligand du CD40 : étude du rôle de son interaction avec le CD40 dans la réponse lymphocytaire B“. Lyon 1, 1995. http://www.theses.fr/1995LYO1T120.

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Evans, Dean E. „CD40 Sustains T Cell Activation During Cognate Communication with Resting B Cells: a Dissertation“. eScholarship@UMMS, 1998. http://escholarship.umassmed.edu/gsbs_diss/178.

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T and B-lymphocytes play an important role in an adaptive immune response. Communication between these two cells may result in either a humoral immune response or tolerance. Communication between T and B-lymphocytes involves a number of inducible cell surface molecules on both T and B-lymphocytes. It was the aim of this project to gain a greater understanding of the role of CD40 in the dynamic communication that occurs between naïve T-lymphocytes and resting B-lymphocytes during cognate communication. Because in vivo antigen specific T-lymphocytes are at low frequency, it is difficult to examine antigen-specific naïve T-lymphocytes. Thus, an in vitro system employing naïve antigen-specific T cell receptor (TCR) transgenic T cells and small resting B-lymphocytes that did not express CD40 was devised to examine the role of CD40 in cognate communication between naïve T-lymphocytes and resting B-lymphocytes. Upon recognition of antigen on resting B-lymphocytes that expressed CD40, T-lymphocytes proliferated, expressed the activation antigens CD69 and CD25, and remained responsive to subsequent antigen challenge. In the absence of CD40, resting B-lymphocytes did not induce sustained proliferation or sustained expression of the activation markers CD69 and CD25 on naïve T-lymphocytes, and their recovery was decreased compared to naïve T-lymphocytes that recognized antigen on resting B-lymphocytes that expressed CD40. Naïve T-lymphocytes, however, remained responsive to subsequent antigen challenge after recognition of antigen on resting CD40-/- B-lymphocytes. Recognition of antigen on resting CD40-/- B-lymphocytes also resulted in increased recovery and antigen responsiveness of T-lymphocytes when compared to controls without antigen, The role of CD40 in sustaining activation of naïve T-lymphocytes may be unique to resting B-lymphocytes, since proliferation of naïve T-lymphocytes in response to dendritic cells that did not express CD40 was similar to proliferation of naïve T-lymphocytes in response to dendritic cells that expressed CD40. The mechanism by which CD40 sustained activation of naïve T-lymphocytes was investigated by examining the induction of various costimulatory molecules on resting CD40+/- and CD40-/- B-lymphocytes during cognate interaction with naive T-lymphocytes. Induction of B7-1, upregulation of CD44 and ICAM-1, and sustained but not initial induction of B7-2 required that CD40 be expressed on resting B-lymphocytes. Expression of B7-1 and CD44H was not required for proliferation of naïve T-lymphocytes in response to antigen presented on resting B-lymphocytes. However, sustained expression of B7-2 was crucial for proliferation of naïve T-lymphocytes in response to antigen presented on resting B-lymphocytes.

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Esquerré, Michael. „Influence des lymphocytes T CD4+ CD25+ régulateurs sur la dynamique de formation de la synapse immunologique entre un lymphocyte T CD4+ effecteur et une cellule présentatrice d'antigène“. Toulouse 3, 2007. http://thesesups.ups-tlse.fr/51/.

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La rencontre entre un lymphocyte T et une cellule présentatrice d'antigène (CPA) est un évènement central dans l'initiation et le développement de la réponse immunitaire adaptative. L'interaction entre ces deux cellules entraîne de nombreuses réorganisations moléculaires au niveau de l'aire de contact intercellulaire conduisant à la formation d'une structure dynamique et spécialisée remplissant diverses fonctions biologiques : la Synapse Immunologique (SI). Cette interaction permet à un lymphocyte T CD4+ helper (TH) de s'activer et de mettre en place une signalisation intracellulaire nécessaire à la production de cytokines. Le second aspect crucial de cette interaction consiste en la polarisation de la machinerie sécrétoire du lymphocyte TH vers la CPA permettant ainsi une activation sélective de la CPA présentant l'antigène spécifique et donc une amplification sélective de la réponse immunitaire. Les lymphocytes T CD4+ CD25+ régulateurs naturels (Treg) jouent un rôle capital dans le maintien de la tolérance périphérique au soi, leur absence conduisant au développement de syndromes lymphoprolifératifs auto-immuns. Les Treg sont également impliqués dans le contrôle des réponses immunitaires anti-infectieuses et ont un rôle délétère lors des réponses immunitaires anti-tumorales. Différents mécanismes de régulation impliquant le contact cellulaire ou bien la sécrétion de molécules effectrices solubles ont à ce jour été décrits. Mon travail de thèse a été de déterminer si les Treg humains pourraient inhiber les réponses immunitaires en altérant la polarisation des lymphocytes TH vers les CPA. Afin de répondre à cette question, nous avons utilisé des approches de microscopie confocale afin de visualiser un Treg et un lymphocyte TH interagissant simultanément avec une même CPA. Nous avons pu observer que les Treg inhibent la polarisation de la machinerie sécrétoire des lymphocytes TH (appareil de Golgi et cytosquelette de tubuline) vers la CPA via la production locale de TGF-bêta. L'obtention de ces résultats nous a permis d'identifier un nouveau mécanisme de suppression, qui pourrait permettre de mieux appréhender l'incroyable potentiel des Treg à réguler finement les réponses immunitaires
The encounter between a T lymphocyte and an antigen presenting cell (APC) is a central event in the initiation and development of adaptative immune responses. Interaction between these two cells leads to multiple molecular reorganizations of the intercellular contact site leading to the formation of a dynamical and specialized structure filling diverse biological functions: the Immunological Synapse (IS). This interaction enables a CD4+ T helper lymphocyte (TH) to activate and to put into place an intracellular sustained signaling necessary for cytokine production. The second key feature of this interaction consists in TH lymphocyte secretory machinery polarization towards APC thereby allowing a selective activation of the APC presenting the specific antigen and thus a selective amplification of the immune response. CD4+ CD25+ natural regulatory T lymphocytes (Treg) play a pivotal role in the maintenance of peripheral self tolerance, their absence leading to the development of autoimmune lymphoproliferative disorders. Treg are also involved in controlling anti-infectious immune responses and have a deleterious role during anti-tumoral immune responses. To date, different regulation mechanisms involving cellular contact or the secretion of soluble effector molecules have been described. My thesis work was to determine if human Treg could inhibit immune responses by altering polarization of TH lymphocytes towards APC. In order to answer this question we used confocal microscopy approaches so as to visualize a Treg and a TH lymphocyte simultaneously interacting with a same APC. We were able to observe that Treg inhibit secretory machinery polarization of TH lymphocytes (Golgi apparatus and tubulin cytoskeleton) towards APC via local TGF- production. These results enabled us to identify a novel suppression mechanism that could allow to better apprehend the incredible potential of Treg to finely regulate immune responses

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Liu, Anquan. „Proinflammatory factor mediated lymphocyte activation - the pivotal role of leukotriene B4 /“. Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-391-7/.

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Jellison, Evan Robert. „CD4 T Cell-Mediated Lysis and Polyclonal Activation of B Cells During Lymphocytic Choriomeningitis Virus Infection: A Dissertation“. eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/349.

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CD4 T cells and B cells are cells associated with the adaptive immune system. The adaptive immune system is designed to mount a rapid antigen-specific response to pathogens by way of clonal expansions of T and B cells bearing discrete antigen-specific receptors. During viral infection, interactions between CD4 T cells and B cells occur in a dynamic process, where B cells that bind to the virus internalize and degrade virus particles. The B cells then present viral antigens to virus-specific CD4 T cells that activate the B cells and cause them to proliferate and differentiate into virus-specific antibody-secreting cells. Yet, non-specific hypergammaglobulinemia and the production of self-reactive antibodies occur during many viral infections, and studies have suggested that viral antigen-presenting B cells may become polyclonally activated by CD4 T cells in vivo in the absence of viral engagement of the B cell receptor. This presumed polyclonal B cell activation associated with virus infection is of great medical interest because it may be involved in the initiation of autoimmunity or contribute to the long-term maintenance of B cell memory. In order to directly examine the interactions that occur between T cells and B cells, I asked what would happen to a polyclonal population of B cells that are presenting viral antigens, if they were transferred into virus-infected hosts. I performed these studies in mice using the well-characterized lymphocytic choriomeningitis virus (LCMV) model of infection. I found that the transferred population of antigen-presenting B cells had two fates. Some antigen-expressing B cells were killed in vivo by CD4 T cells in the first day after transfer into LCMV-infected hosts. However, B cells that survived the cytotoxicity underwent a dynamic polyclonal activation manifested by proliferation, changes in phenotype, and antibody production. The specific elimination of antigen-presenting B cells following adoptive transfer into LCMV-infected hosts is the first evidence that MHC class II-restricted killing can occur in vivo during viral infection. This killing was specific, because only cells expressing specific viral peptides were eliminated, and they were only eliminated in LCMV-infected mice. In addition to peptide specificity, killing was restricted to MHC class II high cells that expressed the B cell markers B220 and CD19. Mice depleted of CD4 T cells prior to adoptive transfer did not eliminate virus-specific targets, suggesting that CD4 T cells are required for this killing. I found that CD4 T cell-dependent cytotoxicity cannot be solely explained by one mechanism, but Fas-FasL interactions and perforin are mechanisms used to induce lysis. Polyclonal B cell activation, hypothesized to be the cause of virus-induced hypergammaglobulinemia, has never been formally described in vivo. Based on previous studies of virus-induced hypergammaglobulinemia, which showed that CD4 T cells were required and that hypergammaglobulinemia was more likely to occur when virus grows to high titer in vivo, it was proposed that the B cells responsible for hypergammaglobulinemia may be expressing viral antigens to virus-specific CD4 T cells in vivo. CD4 T cells would then activate the B cells. However, because the antibodies produced during hypergammaglobulinemia are predominantly not virus-specific, nonvirus-specific B cells must be presenting viral antigens in vivo. In my studies, the adoptively transferred B cells that survived the MHC class II-restricted cytotoxicity became polyclonally activated in LCMV-infected mice. Most of the surviving naïve B cells presenting class II MHC peptides underwent an extensive differentiation process involving both proliferation and secretion of antibodies. Both events required CD4 cells and CD40/CD40L interactions to occur but B cell division did not require MyD88-dependent signaling, type I interferon signaling, or interferon γ signaling within B cells. No division or activation of B cells was detected at all in virus-infected hosts in the absence of cognate CD4 T cells and class II antigen. B cells taken from immunologically tolerant donor LCMV carrier mice with high LCMV antigen load became activated following adoptive transfer into LCMV-infected hosts, suggesting that B cells can present sufficient antigen for this process during a viral infection. A transgenic population of B cells presenting viral antigens was also stimulated to undergo polyclonal activation in LCMV-infected mice. Due to the high proportion of B cells stimulated by virus infection and the fact that transgenic B cells can be activated in this manner, I conclude that virus-induced polyclonal B cell activation is independent of B cell receptor specificity. This approach, therefore, formally demonstrates and quantifies a virus-induced polyclonal proliferation and differentiation of B cells which can occur in a B cell receptor-independent manner. By examining the fate of antigen-presenting B cells following adoptive transfer into LCMV-infected mice, I have been able to observe dynamic interactions between virus-specific CD4 T cells and B cells during viral infection. Adoptive transfer of antigen-presenting B cells results in CD4 T cell-mediated killing and polyclonal activation of B cells during LCMV infection. Studies showing requirements for CD4 T cells or MHC class II to control viral infections must now take MHC class II-restricted cytotoxicity into account. Polyclonal B cell activation after viral infection has the potential to enhance the maintenance of B cell memory or lead to the onset of autoimmune disease.

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Bücher zum Thema "CD44 B-Lymphocytes Lymphocyte Activation"

Sudhir, Gupta, Hrsg. Mechanisms of lymphocyte activation and immune regulation XI: B cell biology. New York: Springer, 2007.

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Grosschedl, Rudolf, und Harinder Singh. Molecular Analysis of B Lymphocyte Development and Activation. Springer, 2014.

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(Editor), Harinder Singh, und Rudolf Grosschedl (Editor), Hrsg. Molecular Analysis of B Lymphocyte Development and Activation (Current Topics in Microbiology and Immunology, No. 290). Springer, 2005.

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1950-, Grinstein Sergio, und Rotstein Ori D, Hrsg. Mechanisms of leukocyte activation. San Diego: Academic Press, 1990.

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(Editor), Sudhir Gupta, Frederick W. Alt (Editor), Max D. Cooper (Editor), Fritz Melchers (Editor) und Klaus Rajewsky (Editor), Hrsg. Mechanisms of Lymphocyte Activation and Immune Regulation XI: B Cell Biology (Advances in Experimental Medicine and Biology). Springer, 2007.

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Hartigan-O’Connor, Dennis J., und Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.

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The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HIV, although immune recovery is quite variable. A subset of patients with AIDS will develop immune reconstitution inflammatory syndromes after initiation of ART. Approximately 1% of persons with HIV are able to control infection without the need for ART (“elite” controllers). A variety of immune-based therapies, including hydroxyurea, growth hormone, and statins, are being studied in clinical trials and may ultimately play a role in treating persons with HIV infection.

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Voll, Reinhard E., und Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.

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Buchteile zum Thema "CD44 B-Lymphocytes Lymphocyte Activation"

Rudd, Christopher E., Elizabeth K. Barber, Kristine E. Burgess, Julie Y. Hahn, Andreani D. Odysseos, Man Sun Sy und Stuart F. Schlossman. „Molecular Analysis of the Interaction of p56lck with the CD4 and CD8 Antigens“. In Mechanisms of Lymphocyte Activation and Immune Regulation III, 85–96. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5943-2_10.

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Laurence, Jeffrey. „CD4+ and CD8+ T Lymphocyte Activation in HIV Infection“. In Advances in Experimental Medicine and Biology, 1–15. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1995-9_1.

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Ambrus, Julian L., Cynthia H. Jurgensen, Debra L. Bowen, Shohken Tomita, Toshimasa Nakagawa, Naoko Nakagawa, Harris Goldstein, Normal L. Witzel, Howard S. Mostowski und Anthony S. Fauci. „The Activation, Proliferation, and Differentiation of Human B Lymphocytes“. In Mechanisms of Lymphocyte Activation and Immune Regulation, 163–75. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5323-2_16.

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Melchers, Fritz, Steven R. Bauer, Christoph Berger, Hajime Karasuyama, Akira Kudo, Antonius Rolink, Nobuo Sakaguchi, Andreas Strasser und Philipp Thalmann. „Precursor B Lymphocytes — Specific Monoclonal Antibodies and Genes“. In Mechanisms of Lymphocyte Activation and Immune Regulation II, 87–93. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-5803-0_11.

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Sutro, Jeffrey B., Bharathi S. Vayuvegula, Sudhir Gupta und Michael D. Cahalan. „Voltage-Sensitive Ion Channels in Human B Lymphocytes“. In Mechanisms of Lymphocyte Activation and Immune Regulation II, 113–22. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-5803-0_14.

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„Second Signals for T Cell Mitogenesis Provided by a MAbs CD45 (T200) and CD5 (T1)“. In Lymphocyte Activation and Differentiation, 549–52. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110850253-083.

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„Studies Regarding the Interaction of the T4 (CD4) Molecule with the Envelope Protein gp120 of the Human Immunodeficiency Virus (HIV)“. In Lymphocyte Activation and Differentiation, 445–48. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110850253-064.

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„Immunobiology of B Lymphocytes“. In Lymphocyte Activation and Differentiation, 553–56. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110850253-084.

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Petersone, Lina, und Lucy S. K. Walker. „Activation of CD4+ T Lymphocytes“. In Cancer Immunotherapy Principles and Practice. 2. Aufl. New York, NY: Springer Publishing Company, 2021. http://dx.doi.org/10.1891/9780826137432.0007.

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„Changes in Gene Expression in Differentiating B Lymphocytes“. In Lymphocyte Activation and Differentiation, 591–94. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110850253-092.

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Konferenzberichte zum Thema "CD44 B-Lymphocytes Lymphocyte Activation"

Carmona, Eva M., Theodore Kottom, Deanne Hebrink und Andrew H. Limper. „CD4-Independent Activation Of Human B Lymphocytes By Pneumocystis Beta-Glucans“. In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3298.

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