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Cheng, Gordon W. "Functions of CD45 in TCR signaling in CD4§+CD8§+ double-positive thymocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29256.pdf.
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Eichelbauer, Dirk. "In-vitro-Untersuchungen zur Stimulation von humanen TZR-[alpha]/[beta]+-CD4-CD8-doppeltnegativen [TZR-alpha-beta-CD4-CD8-doppeltnegativen] T-Lymphozyten." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=970313373.
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Cauchy, Pierre. "Rôle et contexte transcriptionnel du facteur de transcription Ets1 au cours transition CD4- CD8- à CD4+ CD8+ de la tymopoïèse αβ." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22135.
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ETS1 est un facteur de transcription (FT) spécifique transposé dans les leucémies aigües. Le rôle essentiel d'ETS1 a été décrit au cours de l'hématopoïèse, plus particulièrement dans la différenciation lymphocytaire T. Son expression temporelle coordonnée participe au contrôle des transitions du stade double négatif (DN) CD4-/CD8- au stade double positif (DP) CD4+/CD8+jusqu'au stade simple positif (SP) CD4+ ou CD8+. Au cours de l'ontogenèse T, ETS1 transactive notamment l'expression des chaînes β et α du récepteur des cellules T (TCR). Nous avons criblé à grande échelle les cibles d'ETS1 aux stades DN et DP en ChIP-Seq, ainsi que desmarques histone et de l'ARN polymérase II (Pol II). Afin de faciliter nos analyses bioinformatiques, nous avons développé deux logiciels, CoCAS et AmaMineReg, qui permettent d'identifier plus facilement les cibles à partir de données brutes et de discriminer les vrais des faux positifs. Nous avons trouvé 5900 cibles en DN et 3400 en DP, principalement intergéniques dont 2000 sont communes, non caractérisées et correspondent aux gènes induits par la réponse immédiate à la signalisation TCR. Parmi les cibles différentiellement exprimées entre les deux stades, ETS1 active les gènes thymus-spécifiques et réprime les gènes hématopoïétiques non T spécifiques,en fonction de la co-occurrence avec le motif RUNX1. Nous avons également caractérisé très clairement le site de fixation en conditions natives, qui se révèle être CTTCCT.De plus, ETS1 co-localise avec des marques chromatines permissives aux régions inter- et intragéniques,caractérisées par un contenu GC, densité de motifs de fixation de FT (SFFT) et conservation inter-espèces accrusETS1 is a specific transcription factor (TF) transposed in acute leukemias. key role of ETS1 wasdescribed during hematopoiesis, especially in T lymphocyte differentiation. Its temporal expression participates in the coordinated control of phase transitions from the CD4-/CD8-double negative (DN) stage to CD4+/CD8+ double positive (DP) up to CD4 or CD8 single positivestage (SP). During ontogenesis T ETS1 notably transactivates the expression of the alpha and beta chains of the T-Cell receptor (TCR). We performed genome-wide screening of ETS1 at both DN and DP stages via ChIP-Seq, as well as histone hallmarks and RNA polymerase II (PolII). To facilitate computational analysis we developed two new software suites, and COCASAmaMineReg, which allow easier identification of targets from raw data and to discriminate between true and false positives. We found 5900 targets in 3400 in DN and DP, mostly intergenic, out of which 2000 are common, and correspond to uncharacterized genes induced bythe immediate response to TCR signaling. Among targets differentially expressed between thetwo stages, Ets1 activates thymus-specific genes and represses non T-specific haematopoietic genes depending on the co-occurrence with the RUNX1 motif. We also very clearly characterized the binding site in native conditions, which proved to be CTTCCT. Furthermore, Ets1 colocalizes with permissive chromatin marks in inter-and intra-genic regions, characterized byincreased GC content, TF binding motifs (TFBS) density as well as inter-species conservation
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Pinheiro, CatiÃssia Dantas. "CÃlulas CD3+, CD4+, CD8+, CD3-CD16+CD56+ e CD19+ em sangue perifÃrico de pacientes com hansenÃase e indivÃduos saudÃveis." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=16323.
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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgicoA hansenÃase à uma doenÃa granulomatosa, infecto-contagiosa causada pelo Mycobacterium leprae. Trata-se de uma infecÃÃo crÃnica com amplo espectro de respostas imunes celulares em humanos. Possui alto poder infectante e baixo poder patogÃnico. Este estudo tem como objetivo quantificar e comparar leucÃcitos e subpopulaÃÃes de linfÃcitos T totais (CD3+), T auxiliares (CD3+CD4+), T citotÃxicos (CD3+CD8+), B (CD19+) e NK (CD3-CD16+CD56+) em sangue perifÃrico de indivÃduos com hansenÃase e controles saudÃveis. Os pacientes foram provenientes do Centro de Dermatologia D. LibÃnia, Fortaleza-CE, Brasil. A determinaÃÃo do nÃmero de linfÃcitos em cada subpopulaÃÃo foi realizada por citometria de fluxo. A anÃlise estatÃstica foi realizada pelo programa GraphPad Prism 5.0 para Windows com significÃncia estabelecida para valores de p<0,05. à um estudo do tipo caso controle de carÃter observacional, realizado a partir da anÃlise do sangue perifÃrico de indivÃduos com diagnÃstico de hansenÃase e de indivÃduos saudÃveis. A populaÃÃo de pacientes com hansenÃase, sem tratamento foi composta de 15 pessoas. A populaÃÃo de controles saudÃveis foi composta por 29 pessoas. As mÃdias das contagens de LinfÃcitos NK (CD3-CD16+CD56+) no grupo de pacientes com hansenÃase e nos controles saudÃveis, dadas em cÃlulas/mm3, foram, 147(Â113,4) e 378,1 (Â231,7) respectivamente, p = 0,0008. As mÃdias das contagens de LinfÃcitos B (CD19+) no grupo de pacientes com hansenÃase e nos controles saudÃveis, dadas em cÃlulas/mm3, foram, 233,3 (Â85,89) e 115,3 (Â53,01) , respectivamente, p < 0,0001. NÃo foram encontradas diferenÃas estatÃsticas significantes entre as amostras de leucÃcitos, de linfÃcitos T CD3+, linfÃcitos T CD4+ e linfÃcitos T CD8+. Os dados do presente estudo sinalizam que as cÃlulas NK parecem desempenhar papel de relevÃncia na resposta ao M. leprae. O linfÃcito B jà ocupa papel de destaque na resposta imunolÃgica ao M. leprae, sobretudo nas formas lepromatosas, e este estudo reforÃa a importÃncia destas cÃlulas.
Leprosy is an infectious and granulomatous disease caused by Mycobacterium leprae. The aim of this study was to quantify and compare levels of leucocytes and lymphocyte subpopulations (CD3+, CD3+CD4+, CD3+CD8+, CD19+, CD3-CD16+CD56+) in peripheral blood of patients with leprosy and healthy controls. Patients were followed at Centro de Dermatologia D. LibÃnia, Fortaleza-CE, Brasil. Flow cytometry was used to determine numbers of lymphocytes. Statistical analisys was done with GraphPad Prism 5.0 software for windows. P values under 0.05 were considered siginificant.This was an observational case-control study. Fifteen leprosy patients without treatment were evaluated and 29 healthy individuals were included in control group. NK cells (CD3-CD16+CD56+) mean in leprosy patients was 147(Â113,4) and in controls was 378,1 (Â231,7). Comparisson stablished a p value of 0.0008. B lymphocytes (CD19+) mean in leprosy patients was 233,3 (Â85,89) and in controls was 115,3 (Â53,01), with p < 0,0001 . No differences were observed in CD3+ T lymphocytes, CD4+ T lymphocytes and CD8+ T lymphocytes. This study suggests that NK cells may play a role in innate response to M. leprae.
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Pinheiro, Catiússia Dantas. "Células CD3+, CD4+, CD8+, CD3-CD16+CD56+ e CD19+ em sangue periférico de pacientes com hanseníase e indivíduos saudáveis." reponame:Repositório Institucional da UFC, 2013. http://www.repositorio.ufc.br/handle/riufc/15425.
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PINHEIRO, Catiússia Dantas. Células CD3+, CD4+, CD8+, CD3-CD16+CD56+ e CD19+ em sangue periférico de pacientes com hanseníase e indivíduos saudáveis. 2013. 65 f. Dissertação (Mestrado em Patologia) - Faculdade de Medicina, Universidade Federal do Ceará, Fortaleza, 2013.Submitted by denise santos (denise.santos@ufc.br) on 2016-03-09T13:41:07Z No. of bitstreams: 1 2013_dis_cdpinheiro.pdf: 775643 bytes, checksum: 2d4939ef2f883a155737695a2e7c759a (MD5)
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Leprosy is an infectious and granulomatous disease caused by Mycobacterium leprae. The aim of this study was to quantify and compare levels of leucocytes and lymphocyte subpopulations (CD3+, CD3+CD4+, CD3+CD8+, CD19+, CD3-CD16+CD56+) in peripheral blood of patients with leprosy and healthy controls. Patients were followed at Centro de Dermatologia D. Libânia, Fortaleza-CE, Brasil. Flow cytometry was used to determine numbers of lymphocytes. Statistical analisys was done with GraphPad Prism 5.0 software for windows. P values under 0.05 were considered siginificant.This was an observational case-control study. Fifteen leprosy patients without treatment were evaluated and 29 healthy individuals were included in control group. NK cells (CD3-CD16+CD56+) mean in leprosy patients was 147(±113,4) and in controls was 378,1 (±231,7). Comparisson stablished a p value of 0.0008. B lymphocytes (CD19+) mean in leprosy patients was 233,3 (±85,89) and in controls was 115,3 (±53,01), with p < 0,0001 . No differences were observed in CD3+ T lymphocytes, CD4+ T lymphocytes and CD8+ T lymphocytes. This study suggests that NK cells may play a role in innate response to M. leprae.
A hanseníase é uma doença granulomatosa, infecto-contagiosa causada pelo Mycobacterium leprae. Trata-se de uma infecção crônica com amplo espectro de respostas imunes celulares em humanos. Possui alto poder infectante e baixo poder patogênico. Este estudo tem como objetivo quantificar e comparar leucócitos e subpopulações de linfócitos T totais (CD3+), T auxiliares (CD3+CD4+), T citotóxicos (CD3+CD8+), B (CD19+) e NK (CD3-CD16+CD56+) em sangue periférico de indivíduos com hanseníase e controles saudáveis. Os pacientes foram provenientes do Centro de Dermatologia D. Libânia, Fortaleza-CE, Brasil. A determinação do número de linfócitos em cada subpopulação foi realizada por citometria de fluxo. A análise estatística foi realizada pelo programa GraphPad Prism 5.0 para Windows com significância estabelecida para valores de p<0,05. É um estudo do tipo caso controle de caráter observacional, realizado a partir da análise do sangue periférico de indivíduos com diagnóstico de hanseníase e de indivíduos saudáveis. A população de pacientes com hanseníase, sem tratamento foi composta de 15 pessoas. A população de controles saudáveis foi composta por 29 pessoas. As médias das contagens de Linfócitos NK (CD3-CD16+CD56+) no grupo de pacientes com hanseníase e nos controles saudáveis, dadas em células/mm3, foram, 147(±113,4) e 378,1 (±231,7) respectivamente, p = 0,0008. As médias das contagens de Linfócitos B (CD19+) no grupo de pacientes com hanseníase e nos controles saudáveis, dadas em células/mm3, foram, 233,3 (±85,89) e 115,3 (±53,01) , respectivamente, p < 0,0001. Não foram encontradas diferenças estatísticas significantes entre as amostras de leucócitos, de linfócitos T CD3+, linfócitos T CD4+ e linfócitos T CD8+. Os dados do presente estudo sinalizam que as células NK parecem desempenhar papel de relevância na resposta ao M. leprae. O linfócito B já ocupa papel de destaque na resposta imunológica ao M. leprae, sobretudo nas formas lepromatosas, e este estudo reforça a importância destas células.
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Anand, Arthi. "Characterization of CD3+CD4-CD8- (double negative) T cells in patients with systematic lupus erythematosus (SLE)." Thesis, University College London (University of London), 2003. http://discovery.ucl.ac.uk/1445261/.
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Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease characterized serologically by B cell hyperactivity and a panoply of autoantibodies against nuclear, cytoplasmic and cell surface antigens. It is thought that T cells are involved in this process and more recently it has been suggested that the CD4+ CD8+, i.e.double negative (DN) T cells, might be important. As a start to understanding the contribution of DN T cells to disease pathogenesis in SLE, the percentages of DN T cells were determined and it was found that otp but not y5 DNT cells were significantly increased in patients with SLE when compared to rheumatoid arthritis (RA) (autoimmune controls) and healthy controls. To further establish their participation in the autoimmune reactions in SLE, the activation markers expressed by the DN T cells were examined. It was found that HLA-DR and CD69, and co-stimulatory molecules CD28 and CTLA-4 were all expressed by significantly higher percentages of DNT cells from patients with SLE, than those with RA or healthy controls (HC). More DN T cells from SLE patients were CD45RA+ than from controls, while CD45R0+ were reduced. DN T cells in patients with SLE also showed a more activated phenotype than their CD4+/ CD8+ counterparts. To understand the functional significance in SLE DNT cells, the percentages of SLE otp TCR+ DN T cells containing intracellular IL-4, a Th2 cytokine was determined. Higher percentages of SLE ap TCR DN+ T cells contained DL-4 constitutively than RA or HC. DN T cell populations from patients with SLE showed greater resistance to apoptosis in culture than the conventional CD4/CD8+ cells and DN T cells from healthy controls. High Bcl-2/Bax ratios and higher levels of Bcl-x observed in the DN T cells from patients with SLE could explain their resistance to apoptosis compared to the conventional T cells and DN T cells from healthy controls.
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Khan, Qasim. "Regulation of apoptosis in CD4§-CD8§- Ãߧ+ T cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ29310.pdf.
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Tyznik, Aaron Jacob. "CD4+ T cell help for CD8+ T cell responses /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8314.
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Behrendt, Anne. "Differential antigen dependency of CD4+ and CD8+ T cells." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-171521.
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Wheeler, Lee Adam. "CD4 Aptamer-SiRNA Chimeras (CD4-AsiCs) Knockdown Gene Expression in CD4+ Cells and Inhibit HIV Transmission." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10272.
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The continued spread of HIV underscores the need to interrupt transmission. One attractive strategy is a topical microbicide. Sexual transmission of herpes simplex virus type 2 (HSV-2) in mice can be inhibited by intravaginal small inhibitory RNA (siRNA) application. To overcome the challenges of using siRNAs to knock down gene expression in immune cells susceptible to HIV infection, we used chimeric RNAs composed of an aptamer fused to an siRNA for targeted gene knockdown in cells bearing an aptamer-binding receptor. Here, we showed that CD4 aptamer-siRNA chimeras (CD4-AsiCs) specifically suppress gene expression in CD4+ T cells and macrophages in vitro, in polarized cervicovaginal tissue explants, and in both the genital and rectal tracts of humanized mice. CD4-AsiCs do not activate lymphocytes or stimulate innate immunity, provide durable target gene silencing for up to three weeks in vitro, and maintain effectiveness in a hydroxyethyl cellulose (HEC) gel formulation. CD4-AsiCs that knock down HIV genes and/or CCR5 inhibited HIV infection in vitro and in cervicovaginal explants. When applied intravaginally to humanized mice, CD4-AsiCs provided durable protection against transmission of the virus. Thus, CD4-AsiCs could be used as the active ingredient of a microbicide to prevent the sexual transmission of HIV.
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Freitag, Kimberly A. "Effects of Acute Nutritional Deprivation on Lymphocyte Subsets and Membrane Function in Cats." Thesis, Virginia Tech, 1998. http://hdl.handle.net/10919/46484.
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Identification of patients with suboptimal nutritional status allows for early treatment intervention. Currently, no definitive test of nutritional status exists. Therefore, this study was conducted to identify possible functional indicators of acute nutritional deprivation. The effects of total nutritional deprivation and subsequent refeeding on lymphocyte functions and subpopulations were examined in 23 healthy cats. Peripheral blood samples were analyzed at various times during fasting and refeeding periods. During the fasting period, decreases were observed in leukocyte number (day 4; p < 0.04), lymphocyte number (p < 0.02), CD4+ cells (day 4; p < 0.06), CD4:CD8 ratio (0 hours; p < 0.004), and mitogen stimulated CD4:CD8 ratio (72 hours; p < 0.15) during the fasting period as compared to baseline. Increases were seen in CD4+ cells (day 7; p < 0.09), CD8+ cells (day 7; p < 0.04) and intracellular calcium (day 4; p < 0.02) as compared to baseline. During the refeeding period increases (p < 0.05) were observed in leukocyte number, CD4+ cells, CD8+ cells, lymphocyte proliferation (p < 0.07) and lymphocyte number (p < 0.004) as compared to day 7. These findings suggest that 7 days starvation had immunosuppressive effects on cats which were alleviated during 7 days refeeding. The use of CD4:CD8 ratio in conjunction with intracellular calcium flux may be useful as indices of nutritional status.Master of Science
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Parrot, Tiphaine. "Étude des lymphocytes Tαβ double positifs CD4+ CD8+ intra-tumoraux dans la réponse immune anti-mélanome." Thesis, Nantes, 2016. http://www.theses.fr/2016NANT1031/document.
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L’infiltrat immunitaire joue un rôle déterminant dans la progression tumorale et sert d’indicateur quant à la réussite ou à la mise en échec des traitements antitumoraux, notamment dans le cadre des immunothérapies. Une dissection fine de ses composants cellulaires et de leurs interactions est donc fondamentale pour améliorer à terme les essais thérapeutiques. C’est dans ce contexte que notre équipe a identifié parmi les lymphocytes T infiltrant les mélanomes, des lymphocytes Tαβ co-exprimant les récepteurs CD4 et CD8 (LT DP) et réactifs à la tumeur de façon HLA-I restreinte. Nos travaux écartent l’hypothèse d’un rôle cytotoxique ou régulateur de ces cellules et mettent en évidence une fonction de type helper via l’expression de la molécule CD40L. L’interaction CD40L/CD40 permet aux LT DP d’induire la prolifération et la différenciation des lymphocytes B d’une part, et d’autre part, de promouvoir la maturation de cellules dendritiques capables d’induire efficacement une réponse lymphocytaire cytotoxique contre des antigènes tumoraux. Par ailleurs, nos travaux attribuent un rôle à la cytokine IL-9 dans la modulation fonctionnelle et dans l’homéostasie des LT DP. Nous montrons que via le récepteur à l’IL-9 exprimé par les LT DP, l’IL-9 impacte positivement leur survie et leur prolifération. De plus, l’IL-9 optimise leur réactivité face à la tumeur en potentialisant leur production cytokinique, en augmentant leur potentiel tumoricide et vraisemblablement leur fonction helper. Il serait désormais intéressant d’évaluer ex vivo la pertinence de ces cellules dans la réponse immune antitumorale en corrélant leur fréquence à l’évolution clinique du patientThe immune infiltrate is a key factor in the tumor progression and has a prognostic value for the efficacy of anti-tumor treatments especially for immunotherapies. Therefore, the understanding of the cellular components and their interactions taking place within the tumor microenvironment is necessary for the future optimization of anti-tumor therapeutic strategies. We previously documented among melanoma-infiltrating lymphocytes, an atypical tumor reactive and class-Irestricted T cell population co-expressing both CD4 and CD8 co-receptors. In this study, we excluded a cytotoxic and regulatory function for these cells and ascribed helper properties through the expression of the CD40L costimulatory molecule. Through the CD40L/CD40 interaction, DP T cells allow B cell proliferation and differentiation, as well as, the licensing of dendritic cells for the efficient priming of an anti-tumor cytotoxic CD8 T cell response. Also, our results described a potential role of the interleukin-9 cytokine in DP T cell function and homeostasis. Through its interaction with its cognate receptor, the IL-9 receptor, expressed by DP T cells, IL-9 increases their survival and proliferation and could enhance their enrichment in the tumor microenvironment. In addition, IL-9 enhances their functional properties including cytokine production, cytolytic activity and probably their helper potential. It would be interesting to now define the relevance of this population ex vivo in the anti-tumor immune response by correlating their intra-tumor frequency with the clinical status of the patients
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郑健 and Jian Zheng. "Generation of human allo-antigen specific CD4+ and CD8+ regulatory T cells with CD40-activated B cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46922969.
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Rabenstein, Hannah. "Antigenabhängige und -unabhängige Proliferation von CD4- und CD8-T-Zellen." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-169430.
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Steinke, Farrah Christine. "Novel roles for TCF-1 and LEF-1 in directing CD4+ T cell fate and silencing CD4 in CD8+ T cells." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1764.
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CD4+ and CD8+ T cells, the essential mediators of cellular immune responses, are produced in the thymus following sequential maturation stages. Hematopoietic progenitors first seed the thymus and make T cell lineage specification and commitment decisions within the CD4−CD8− double negative (DN) compartment. Thymocytes then mature to the CD4+CD8+ double positive (DP) stage, followed by vigorous negative and positive selection processes. The positively selected DP thymocytes first give rise to CD4+CD8lo intermediate (IM) cells which then differentiate into MHC class II-restricted CD4+ and MHC class I-restricted CD8+ T cells, a crucial decision known as CD4+ vs. CD8+ lineage choice.
The lineage choice decision is influenced by the timing, intensity, and duration of signals derived from the TCR and cytokines, and recent studies have identified a number of transcriptional factors that intrinsically regulate this critical fate decision. Among these, Th-POK (encoded by Zbtb7b, called Thpok here for simplicity and consistency with the literature) is specifically required for CD4+ differentiation while Runx factors promote CD8+ T cell production and repress Cd4 in CD8+ lineage committed cells. Upregulation of Thpok is most evident in the CD4+8lo IM cells and is required to antagonize Runx3 activity and expression to promote CD4+ lineage commitment. Collectively, the Th-POK-Runx3 axis appears to be a critical convergence point in the CD4+ vs. CD8+ lineage choice.
After committing to either CD4+ or CD8+ thymocytes, lineage-inappropriate genes are silenced to ensure the distinct identity and functional divergence between these two cell types. Repression of the Cd4 gene on CD8+ lineage committed cells is mediated by a ~430 bp silencer sequence in its first intron. Likewise, Thpok is repressed in CD8+ T cells by a ~560 bp sequence upstream of the Thpok exon 1a, and both Cd4 and Thpok silencers contain consensus binding motifs for Runx factors, which are necessary for CD8+ lineage commitment.
T cell factor 1 (TCF-1) and lymphoid enhancer binding factor 1 (LEF-1) are members of the TCF-LEF family transcription factors and abundantly expressed in T lineage cells, and known to be necessary for the maturation of DN T cells to the DP stage. However, because germline deletion of TCF-1 and LEF-1 causes severe early T cell developmental block and embryonic lethality, respectively, their roles beyond the DP stage are unknown. In my thesis work, I overcame these obstacles by conditionally ablating both TCF-1 and LEF-1 in DP thymocytes using CD4-Cre. We observed impaired differentiation of CD4+ T cells from the bipotent DP precursors in the absence of TCF-1 and LEF-1. Mechanistically, TCF-1 promotes CD4+ T cell development by positively regulating the expression of Thpok. TCF-1 and LEF-1 deficiency also results in derepression of the CD4 co-receptor in CD8+ lineage committed cells. In CD8+ T cells, TCF-1 interacts with Runx3 to repress expression of Cd4. These findings not only broaden the spectra of TCF-LEF-mediated regulatory activities in late stages of T cell development, but also reveal new paradigms in T cell fate decision and identity maintenance.
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Beyers, Albertus Daniel. "Transmembrane signalling by the CD2 and CD4 molecules of T lymphocytes." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291324.
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Helbert, Matthew Reginald. "HIV infection in sub-populations of CD4+ lymphocytes defined by CD45." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261804.
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Dembele, Bamory. "Mécanismes de l'aide lymphocytaire T CD4 aux cellules T CD8 mémoires." Paris 11, 2010. http://www.theses.fr/2010PA11T076.
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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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Jaafoura, Salma. "Mémoire lymphocytaire T et persistance virale." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA114847.
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Au cours d’une réponse immunitaire primaire, les lymphocytes T CD8 mémoires émergent à partir d'un environnement de forte activation immunitaire. Les cellules régulatrices T CD4 FoxP3+ (LTregs) jouent un rôle clé de suppression de la réponse immunitaire. Nous montrons que les LTregs sont nécessaires pour la génération d’une réponse mémoire T CD8 fonctionnelle. En absence de LTregs lors du priming, les LT CD8 mémoires générées prolifèrent faiblement et ne parviennent pas à se différencier après une réactivation antigénique en effecteurs cytotoxiques secondaires fonctionnelles. Nous suggérons que les LTregs agissent tôt, lors de la phase d'expansion des LT CD8, en réduisant l’exposition des précurseurs mémoires T CD8 à l'interleukine-2. Ce nouveau rôle crucial des LTregs a des implications pour le développement optimal de vaccin.Chez les patients sous traitement antirétroviral efficace et prolongée (ART), le VIH peut persister dans un petit pool de cellules T CD4 mémoires quiescentes de longue durée de vie infectées par du virus latent intégré. Ce réservoir latent comprend différentes sous-populations mémoires. Nos résultats suggèrent une contraction progressive de la taille du réservoir latent autour d'un noyau formé de sous-populations T CD4 mémoires moins différenciées (centrales mémoires TCM et souches mémoires TSCM). Ce processus très lent semble dépendre de la taille initiale et du taux de décroissance qui diffère entre les sous-populations mémoires infectées de manière latente. Nos résultats suggèrent également une extrême stabilité du sous-réservoir TSCM, dont la taille est directement liée à l'exposition cumulée au virus plasmatique avant le début du traitement ART, soulignant l'importance d'une initiation précoce du traitement antirétroviral efficace. La présence de cette dynamique intrinsèque dans le réservoir latent peut avoir des implications pour la conception de stratégies optimales de purge thérapeutique contre le VIHDuring the primary immune response, CD8 memory emerges from an environment of strong immune activation. The FoxP3 regulatory CD4 T-cell subset (Treg) is known as a key suppressive component of the immune system. We report that Tregs are required for the generation of functional CD8 memory. In the absence of Tregs during priming, the resulting memory cells proliferate poorly and fail to differentiate into functional cytotoxic secondary effectors following antigen reactivation. We find that the Tregs act early, during the expansion phase of primary CD8 effectors, by fine tuning interleukin-2 exposure of CD8 memory precursors. This crucial new role of Tregs has implications for optimal vaccine development. In patients who are receiving prolonged antiretroviral treatment (ART), HIV can persist within a small pool of long-lived resting memory CD4 T cells infected with integrated latent virus. This latent reservoir involves distinct memory subsets. We provide results that suggest a progressive reduction of the size of the blood latent reservoir around a core of less-differentiated memory subsets (central memory and stem cell-like memory).This process appears to be driven by the differences in initial sizes and decay rates between latently infected memory subsets. Our results also suggest an extreme stability of the TSCM sub-reservoir, the size of which is directly related to cumulative plasma virus exposure before the onset of ART, stressing the importance of early initiation of effective ART. The presence of these intrinsic dynamics within the latent reservoir may have implications for the design of optimal HIV therapeutic purging strategies
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Köchling, Annabel. "Postoperative Komplikationen bei HIV-Patienten unter besonderer Berücksichtigung des CD4/CD8-Quotienten." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968081045.
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Yang, Jason D. "Antigen Specific CD4+ and CD8+ T Cell Recognition During Mycobacterium Tuberculosis Infection." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/968.
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Mycobacterium tuberculosis (Mtb) causes human tuberculosis, and more people die of it than of any other pathogen in the world. Immunodominant antigens elicit the large majority of T cells during an infection, making them logical vaccine candidates. Yet, it is still unknown whether these immunodominant antigen-specific T cells recognize Mtb-infected cells. Two immunodominant antigens, TB10.4 and Ag85b, have been incorporated into vaccine strategies. Surprisingly, mice vaccinated with TB10.4 generate TB10.4-specific memory CD8+ T cells but do not lead to additional protection compared to unvaccinated mice during TB. Ag85b-specific CD4+ T cells are also generated during vaccination, but the literature on whether these cells recognize Mtb-infected cells is also inconsistent.
We demonstrate that TB10.4-specific CD8+ T cells do not recognize Mtb-infected cells. However, under the same conditions, Ag85b-specific CD4+ T cells recognize Mtb-infected macrophages and inhibit bacterial growth. In contrast, polyclonal CD4+ and CD8+ T cells from the lungs of infected mice can specifically recognize Mtb-infected macrophages, suggesting macrophages present antigens other than the immunodominant TB10.4. The antigen location may also be critical for presentation to CD8+ T cells, and live Mtb may inhibit antigen presentation of TB10.4. Finally, we propose that TB10.4 is a decoy antigen as it elicits a robust CD8+ T cell response that poorly recognizes Mtb-infected macrophages, allowing Mtb to evade host immunity.
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Li, Ming 1957. "Generation of CD8+ T cell immunity with help from CD4+ T cells." Monash University, Dept. of Pathology and Immunology, 2002. http://arrow.monash.edu.au/hdl/1959.1/8476.
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Hackenbroch, Jessica. "CD4⁺ and CD8⁺ naïve T-cell homeostasis in primary progressive multiple sclerosis." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112629.
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Multiple Sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system. The etiology of MS is unknown but many researchers believe that it is autoimmune mediated. This study investigated naive CD4+ and naive CD8+ T-cell homeostasis in patients with Primary Progressive Multiple Sclerosis and Relapsing Remitting Multiple Sclerosis. The naive T-cell compartment involves a balance between thymic production of naive T-cells, homeostatic proliferation and the delivery of death and survival signals. Naive T-cell production was quantified by measuring signal joint T-cell receptor excision circles (sj-TRECs); episomal byproducts formed during V(D)J T-cell receptor rearrangement.Homeostatic proliferation was quantified by flow cytometry analysis of % expression of CD31 and Ki-67. CD31 is a marker found on CD4+ recent thymic emigrants (RTE) but not on naive T-cells that have undergone homeostatic proliferation. CD31 can be used as a marker of the proliferation history of naive CD4+ T-cells. Ki-67 is a nuclear and nucleolar antigen found in actively cycling cells. It can be used as a marker of cell proliferation at the moment of isolation. Cell survival was measured by quantifying plasma IL-7 levels and by measuring Bcl-2 expressions. IL-7 plays an important role in maintaining and restoring peripheral naive T-cell homeostasis. It stimulates naive T-cell proliferation and prevents the reduction of Bcl-2, an antiapoptotic protein.
In this study, PPMS patients had significantly reduced naive CD4 + T-cell sj-TRECs compared to healthy controls (p = 0.0007) and compared to RRMS patients (p = 0.0010). RRMS patients had fewer sj-TRECs than healthy controls but this difference was not significant (p = 0.4652). Similarly, in PPMS, naive CD4+ T-cells had significantly lower CD31 expression than healthy controls (p = 0.0017) and RRMS patients (p = 0.0032). This finding indicates increased homeostatic proliferation in naive CD4 + T-cells in PPMS, most probably a response to decreased thymic export as marked by the decreased naive CD4+ T-cell sj-TRECs. % CD31 expression in naive CD4+ T-cells did not differ significantly in RRMS compared to healthy controls (p = 0.7455) which is consistent with their naive CD4+ sj-TREC levels.
Naive CD8+ T-cell sj-TRECs were significantly reduced in PPMS patients compared to healthy controls (p = 0.0212) but not compared to RRMS patients (p = 0.2379). RRMS patients had fewer naive CD8 + T-cell sj-TRECs compared to healthy controls but this difference was not significant (p = 0.1517). PPMS patients expressed increased Bcl-2 levels in their naive CD8+ T-cells. This finding indicates upregulation of survival signals, most probably a consequence of reduced thymic export of naive CD8+ T-cells.
The data from this study indicate that PPMS is different from RRMS in their naive CD4+ T-cell sj-TRECs and naive CD4 + T-cell % CD31 expression but is similar to RRMS in their naive CD8+ T-cell sj-TRECs. This study concludes, therefore, that both PPMS and RRMS patients have altered naive T-cell homeostasis.
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Lin, Ya-Ling. "CD4⁺/CD8⁺ T cells and macrophage-derived TNF-α in murine schistosomiasis." Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627622.
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Bronnimann, Heather. "Functional Analysis of Interactions within the TCR-CD3-pMHC-CD4 Macro-complex." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/612427.
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CD4⁺ T cells are a critical component of the adaptive immune compartment. Each T cell expresses a clonotypic T cell receptor (TCR) that must discriminate between self and foreign peptides presented in major histocompatibility molecules (pMHC) on the surface of antigen presenting cells to direct T cell fate decisions. Information regarding TCR-pMHC interactions must then be transmitted to the TCR-associated CD3 signaling modules, which contain ITAMs that serve as signaling substrates for Src kinases. The Src kinase, Lck, is recruited to the pMHC-bound TCR-CD3 complex via association with the CD4 coreceptor that binds MHCII. It is therefore through the coordinated interactions within the TCR-CD3-pMHC-CD4 macro-complex that productive TCR signaling can occur to inform T cell activation and fate decisions. While much is known regarding the structure of the individual subunits that make up the TCR-CD3-pMHC-CD4 macro-complex, there is little information regarding how these components come together to initiate TCR signaling and determine functional outcomes. Here, we have interrogated how interaction of these individual components leads to productive T cell activation. Specifically, we interrogated the nature of TCR-MHC interactions and provide evidence that there is intrinsic specificity of the TCR for MHCII. We have also built mouse models to determine the role of TCR-CD3 interactions and TCR dimerization in the transmission of information from the TCR to the CD3 subunits following TCR-pMHC engagement. Finally, we show that both the CD4 transmembrane and extracellular domains contribute to T cell activation in vitro. Overall, this work provides insight into how the constituents of the TCR-CD3-pMHC-CD4 macro-complex interact to initiate T cell fate and function.
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Cariou, Anne. "Spécificité de l'aide T CD4 lors de la réponse T CD8 mémoire." Paris 6, 2009. http://www.theses.fr/2008PA066730.
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Yang, Rui. "Role Of Interleukin-6 In Cd4 And Cd8 T Cell Effector Functions." ScholarWorks @ UVM, 2016. http://scholarworks.uvm.edu/graddis/654.
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IL-6 is an inflammatory cytokine that contributes to the pathogenesis of many immunological diseases including rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, allergic asthma, as well as the protection against infections caused by various pathogens. These are linked to its role in regulating CD4 T cell differentiation and effector function.
Most of these functions are dependent on the IL-6-mediated signaling through the transcription factor Stat3. In this thesis, we identify a novel molecular mechanism by which IL-6 regulates CD4 T cell effector function. We show that IL-6-dependent signal raises the levels of mitochondrial Ca2+ late during activation of CD4 T cells. This is further used to prolong the expression of effector cytokines IL-4 and IL-21. The modulation of mitochondrial Ca2+ is mediated by the regulation of mitochondrial Stat3 and the formation of respiratory supercomplexes. Thus, in addition to the canonical signaling of IL-6 through Stat3 as a transcription factor, IL-6 also modulates mitochondrial Stat3 to regulate mitochondrial function in CD4 T cells. This could be an alternative pathway by which IL-6 regulates effector function of CD4 T cells and it could contribute to the pathogenesis of inflammatory disease.
Little is known about the effects of IL-6 on CD8 T cells. In this thesis, we reveal a paradigm-shifting mechanism by which IL-6 regulates antibody production by converting CD8 T cells into B cell helpers through IL-21. Briefly, IL-6 promotes the differentiation of a subset of naïve CD8 T cells into a unique population of effector CD8 T cells characterized by the production of high levels of IL-21. IL-21-producing CD8 T cells provide help to B cells to induce isotype switching and protective antibody production during infection.
In summary, this thesis provides new insights into both mechanistic and functional aspects of IL-6 in regulating T cell function. These findings may shed light on the development of new therapeutic approaches in treating autoimmune disorders and preventing infectious diseases.
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Piapi, Alice. "Characterisation of CD3-enhanced gene-modified CD4+ T cells for cancer immunotherapy." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10026088/.
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TCR gene transfer is used to redirect the antigen specificity of T lymphocytes towards known tumour antigens. TCR gene therapies in murine studies have shown promising results. However, in the clinic they have often generated sub-optimal responses, when compared to treatments with tumour infiltrating lymphocytes. Previous work to improve TCR gene therapy has demonstrated that transferring additional CD3 genes increases TCR expression of both endogenous and introduced TCR, in CD4+ and CD8+ T cells. In vivo experiments demonstrated that CD8+ T cells, transduced with TCR and additional CD3 were more effective in tumour protection than T cells transduced with the TCR alone. In this thesis the effects of CD3 (and as a consequence TCR) overexpression were studied in CD4+ and CD8+ T cells, that had been transduced with a retroviral vector containing the CD3 chains genes (CD3-GFP). In vitro analysis showed that CD4+ T cell expressed higher levels of TCR compared to CD8+ T cells, both before and after transduction with the CD3-GFP vector. This associated with higher Ca2+ and CD107a concentration, but no difference in T cell activation or proliferation. Unexpectedly, we found that increased TCR expression did not improve T cell functional avidity following polyclonal or peptide-specific stimulation. In vivo CD3-enhanced CD4+ T cells survived for longer and were recovered in higher percentages, compared to CD3-enhanced CD8+ T cells and mock transduced CD4+ T cells, both in non-competition and competition experiments. Interestingly, this was observed despite a down-regulation of TCR levels in the CD3-enhanced CD4+ T cells, compared to their pre-transfer TCR levels, which was not observed in the control-transduced CD4+ T cells. The mechanism that drives TCR down-regulation and its biological meaning are unknown and require further investigation.
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URGELL, LAFONT PASCALE. "Evolution des populations lymphocytaires cd4+ et cd8+ dans le sang au cours de la polyarthrite rhumatoide : etude longitudinale a propos de 39 cas." Toulouse 3, 1992. http://www.theses.fr/1992TOU31005.
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Andoins, Catherine. "Tolérance aux allogreffes cardiaques le rat après traitement par le LF08. 0299 : étude des mécanismes d'induction et de maintien." Dijon, 1997. http://www.theses.fr/1997DIJOS054.
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La compréhension des mécanismes de rejet et de tolérance des allogreffes est à ce jour encore incomplète. En outre, l'induction de la tolérance en transplantation reste chez l'homme un but à atteindre. Le LF08-0299, Tresperimus, est un nouvel immunosuppresseur capable d'induire une tolérance spécifique a une allogreffe chez l'animal. L'objet du travail de thèse a été l'étude de cette tolérance, induite à l'aide d'un traitement de courte durée par le LF 08-0299 (J1-J20, 6 mg/kg/jours, i. P. ), dans un modèle de greffe cardiaque allénique totalement histoincompatible (DA - LEW). Cette étude a permis d'analyser deux points différents : la phase de maintien de la tolérance et la phase d'induction de la tolérance lors du traitement immunosuppresseur. L'analyse du maintien de la tolérance montre qu'elle ne semble liée ni à une délétion clonale, ni à une anergie, ou à une activité veto. En revanche, des cellules suppressives spécifiques CD4+ CD45RC+/- semblent avoir un rôle prépondérant dans ce modèle. Cette activité suppressive présente les caractéristiques de la tolérance infectieuse. En outre, les cellules suppressives sont capables de contrôler le rejet induit par des cellules sensibilisées contre la greffe, même en présence d'IL2 exogène. Ainsi, nous montrons que l'activité suppressive est un mécanisme actif et dominant dans lequel la compétition pour des ligands tels que l'IL2 ne semble pas être un événement clé. L'analyse de l'induction de la tolérance indique que l'infiltrat leucocytaire est très significativement réduit chez les animaux traités. La population macrophagique, majoritaire, est la plus atteinte par le traitement. L'étude des cytokines transcrites intragreffe montre que la tolérance induite par le LF 08-0299 n'est pas liée a une déviation immune de cellules Th1 vers des Th2. De plus, la transcription de ces différentes cytokines Th n'est pas (IL2, IL4, IL13) ou peu (IFNGamma) modifiée, par rapport aux animaux non traités. Le LF 08-0299 ne semble donc pas agir au niveau de l'activation lymphocytaire. En revanche, les messagers de type macrophagique (IL1 alpha et béta, IL6, IL10, GMCSF, iNOS) sont tous réduis chez les animaux traités par rapport aux non traités. Ainsi, le LF 08-0299 présente un profil tout à fait original par rapport aux immunosuppresseurs classiquement utilisés tel que la cyclosporine A.
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Mischke, Dirk. "Generierung regulatorischer T-Zellen aus naiven CD4+-CD45RA+-T-Zellen durch Anti-CD4-Interaktion." Berlin wvb, Wiss. Verl, 2007. http://www.wvberlin.de/data/inhalt/mischke_dirk.html.
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Nishioka, Tomohisa. "CD4[+]CD25[+]Foxp3[+] T cells and CD4[+]CD25[-]Foxp3[+] T cells in aged mice." Kyoto University, 2007. http://hdl.handle.net/2433/135647.
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Haipek, Katia. "Avaliação das subpopulações de linfócitos T CD4+, linfócitos T CD8+ e da razão CD4+/CD8+ em gatos com gengivite crônica e infectados naturalmente pelo vírus da imunodeficiência dos felinos (FIV)." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-25052007-143025/.
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A gengivite crônica e intratável observada em gatos infectados pelo vírus da imunodeficiência felina (FIV) é um problema bastante freqüente na clínica de pequenos animais. O papel do FIV na etiologia da estomatite persistente ainda está por ser determinado. As manifestações orais são freqüentemente os primeiros sintomas observados em pacientes humanos infectados pelo HIV e podem ser usadas como indicadores da progressão da doença. O objetivo do presente estudo foi quantificar os linfócitos T CD4+, T CD8+ e a razão CD4+/CD8+ em uma colônia de gatos com gengivite crônica e naturalmente infectados pelo FIV. Para tanto, foram utilizados 20 gatos, todos apresentando gengivite com graus variando de 1 a 4. Desse total, 10 gatos não eram infectados pelo FIV e os outros 10 felinos eram infectados pelo FIV. Utilizou-se como controle 20 gatos sem gengivite, sendo 10 infectados pelo FIV e outros 10 não infectados pelo Retrovírus. As contagens dos linfócitos T CD4+ e CD8+ foram realizadas utilizando-se a técnica de citometria de fluxo. Os resultados obtidos demonstraram que os gatos com gengivite e infectados pelo FIV apresentaram uma contagem significativamente menor de linfócitos T CD4+ quando comparado aos gatos com gengivite e não infectados pelo FIV. Não houve diferença significativa na contagem de linfócitos T CD8+ entre os gatos com gengivite, infectados ou não pelo FIV. A razão CD4+/CD8+ também se mostrou em declínio nos gatos com gengivite e infectados pelo FIV. Concluiu-se que nas condições do presente estudo, a infecção pelo FIV compromete a resposta imunológica de felino diante da inflamação gengival.Chronic and intractable gingivitis in FIV-infected cats is a relatively common clinical problem in veterinary practice. The role of FIV in the etiology of persistent stomatitis is still undetermined. Oral manifestations often found in HIV-infected people are frequently the first clinical sign of the infection and can be considered as an indicator of the progression of the HIV infection. The purpose of this study was to evaluate the CD4+ and CD8+ T-lymphocytes count and CD4+:CD8+ ratio in a colony of cats with chronic gingivitis. To achieve these goals, a colony of twenty domestic shorthair cats was used. All cats had some degree of gingival inflammation with scores ranging from 1 through 4. Ten cats were FIV-positive and ten were FIV-negative. As a control, twenty cats without gingivitis were used (ten cats were FIV-positive and ten were FIV-negative). CD4+ and CD8+ T-lymphocytes counts were performed by means of flow cytometry in all forty cats and results compared. The results showed that cats with gingivitis and FIV-infected had a lower CD4+ T cells count than cats with gingivitis but not FIV-infected. There was no difference in CD8+ T lymphocytes count among the cats with gingivitis infected or not with the FIV. The CD4+:CD8+ ratio was lower in cats with gingivitis and FIV-infected. One can conclude that FIV infection induces immunological disorders in cats with gingival inflammation.
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Sun, Joseph C. "The role of CD4 T cell help during the CD8 T cell response /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/8334.
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Turqueti, Neves Adriana. "Recognition of renal cell carcinoma by CD8+ and CD4+ TCR-engineered T lymphocytes." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-128858.
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Li, Li. "Induction and regulation of delayed type hypersensitivity by CD4 and CD8 T subsets." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23017.pdf.
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Drews, Lisann Marie [Verfasser]. "Charakterisierung sekretorischer Lysosomen aus humanen CD4+ und CD8+ T-Zellen / Lisann Marie Drews." Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1179184254/34.
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Sousa, Maria da Gloria Teixeira de. "Caracterização das funções dos linfócitos T CD4+ e T CD8+ na cromoblastomicose experimental." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-05012018-095528/.
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A cromoblastomicose é uma infecção fúngica subcutânea causada por fungos da família Dematiceae sendo o principal agente etiológico o fungo Fonsecaea pedrosoi (F. pedrosoi). Estes fungos induzem uma lesão crônica na pele de freqüente recidivas. O objetivo do trabalho foi avaliar alguns aspectos imunológicos na cromoblastomicose experimental através de dois modelos de infecção pelas vias: intraperitoneal (i.p.) e subcutânea (s.c.). No primeiro modelo de infecção pela via s.c. em camundongos BALB/c infectados com 106 conídios de F. pedrosoi, ocorreu a cura espontânea da infecção em aproximadamente 4 semanas. Na subtipagem de linfócitos T em linfonodos regionais ocorreu um predomínio de células T CD4+ que foi constante até a 4ª semana de infecção, no entanto, observamos aumento significativo de linfócitos T CD8+ ao longo da infecção sugerindo que essa população tenha também uma importante participação no controle da doença. Os ensaios de linfoproliferação demonstraram, na 1ª semana de infecção, elevado índice de proliferação celular quando as células de linfonodos foram estimuladas in vitro com antígenos de F. pedrosoi, além da liberação principalmente da citocina IFN-γ, já na 4ª semana de infecção não foi detectado proliferação celular. Esses resultados sugerem que no início da infecção a resposta celular seja mediada principalmente por linfócitos T CD4+ produtores de IFN-γ, o que nos sugere, que neste modelo experimental, polarize uma resposta de células T do tipo Th1. No segundo modelo de infecção, via intraperitoneal (i.p.), camundongos BALB/c infectados com 106 conídios de F. pedrosoi mostraram desenvolvimento de infecção crônica com preservação da imunidade celular mesmo após a 8ª semana. Ainda pela via i.p., os camundongos C57BL/6 nocautes de T CD4+ apresentaram uma maior carga fúngica no início da infecção e em tempos mais tardios a carga fúngica foi semelhante aos camundongos controles (C57BL/6); esses mesmos animais nocautes não apresentaram uma ativação da resposta celular medida pelo teste de HTT (Hipersensibilidade do Tipo Tardio). Quando avaliamos o padrão de citocinas, a citocina IFN-γ produzida pelos órgãos baço e fígado apresentou menores níveis no início da infecção quando comparado ao camundongos controle. Já os níveis de IL-10 aumentaram gradativamente ao longo da infecção e IL-4 não apresentou diferenças em relação ao controle. Nos camundongos nocautes para coa (C57BL/6 CD8 \"KO\"), a carga fúngica, os níveis de citocinas e o teste de HTT foram semelhantes aos animais controle. Esses resultados mostraram que pela via i.p. os linfócitos T, principalmente células T CD4+ são importantes no controle inicial da infecção. Em tempos mais tardios a infecção foi controlada mesmo em camundongos deficientes de linfócitos TCD 4+ ou T CD8+, sugerido que outras células como macrófagos ou NK, estariam atuando de forma mais efetiva no controle da infecção.Abstract not available.
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Morel, Patricia. "Administration d'anticorps monoclonaux anti-cd4 ou anti-cd5 en transplantation renale chez l'homme." Lyon 1, 1990. http://www.theses.fr/1990LYO1M170.
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Drews, Lisann [Verfasser]. "Charakterisierung sekretorischer Lysosomen aus humanen CD4+ und CD8+ T-Zellen / Lisann Marie Drews." Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1179184254/34.
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Takayama, Eiji. "Enhancement of Activation-Induced Cell Death by Fibronectin in Murine CD4[+]CD8[+] Thymocytes." Kyoto University, 2001. http://hdl.handle.net/2433/150598.
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Böttler, Tobias Elmar. "Rolle von CD4 +CD2 5+ regulatorischen T-Zellen bei der chronischen HCV-Infektion." [S.l. : s.n.], 2005.
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Rose, Charlotte S. P. "CD4 antigen chimaeras of poliovirus." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240217.
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Піддубна, Анна Іванівна, Анна Ивановна Поддубная, Anna Ivanivna Piddubna, Микола Дмитрович Чемич, Николай Дмитриевич Чемич, and Mykola Dmytrovych Chemych. "Залежність клінічних проявів СНІДу від рівня CD4-клітин." Thesis, Видавництво СумДУ, 2010. http://essuir.sumdu.edu.ua/handle/123456789/5145.
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Silva, Pedro Mário Lemos da. "Associação entre a atividade sexual e marcadores de imunidades adquirida em mulheres com AIDS em um município do Nordeste brasileiro." Universidade Federal do Maranhão, 2015. http://tedebc.ufma.br:8080/jspui/handle/tede/1026.
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Previous issue date: 2015-04-30INTRODUCTION:The Acquired Immunodeficiency Syndrome (Aids) comes along the years promoting inversion of the relation men/women in the age group of 13 to 19 years, committing mainly the reproductive life phase women. The sexuality, inherent upon human being, has in the expression of satisfaction of the sexual performance the possibility of providing several benefits in the quality of life of people, such as increase of the longevity, among others. In women living with Aids the main marker of immunity are the CD4+ T lymphocytes used for evaluating the need of antiretroviral therapy (ARVT). OBJECTIVE: Showing up the association between the CD4 count and the sexual performance of women living with Aids in Imperatriz city. METHODOLOGY: cross-sectional study, carried out in the period of march, 2014 to december, 2014, in which it was selected women with diagnosis of Aids, using ARVT at least six months before interview, originating from the Specialized Aids Service (SAS), registered in the Medicines Logistic Control System - SICLOM, of Imperatriz town. They were included those women older than 18, who related having sexual practice before the diagnosis of Aids, capable of communicating, without any cognitive deficit. The facts about the socio-demographic and behavioral variables, clinical factors related to co-morbidities were recorded in own form, right away they answered the Female Sexual Function Index (FSFI) questionnaire. The sample was based in the quantitative of women registered in the SICLOM of Imperatriz Town, sampling error of 5%, confidence interval (CI) of 95%, alpha value ≤ 5%. The chisquare test was used to evaluate the association between the variables, so the Kruskal- Wallis test when necessary. The test of Spearman was utilized for showing the correlation between the relation CD4/CD8 and FSFI. RESULT: the sample included 149 women, it was noted that the larger FSFI score means and medians coincided with the highest means of CD4 T- lymphocyte count from the 2rd quartile (Kruskal Wallis test, p = 0.0347), and there was a positive association between FSFI and the CD4 / CD8 ratio (p = 0.0264), confirming the alternative hypothesis (Spearman correlation). CONCLUSION: It was concluded there is a positive association between the sexual performance and CD4 count.
INTRODUÇÃO: A Síndrome da Imunodeficiência Adquirida (Aids) vem ao longo dos anos promovendo inversão da relação homem/mulher na faixa etária de 13 a 19 anos, comprometendo principalmente as mulheres na fase de vida reprodutiva. A expressão de satisfação no desempenho sexual possibilita proporcionar vários benefícios na qualidade de vida como o aumento da longevidade. Na Aids o principal marcador de imunidade são os linfócitos T-CD4, usados para avaliar a necessidade de terapia antirretroviral (TARV). OBJETIVO: identificar associação da concentração dos linfócitos T-CD4 e o desempenho sexual das mulheres com Aids do município de Imperatriz. METODOLOGIA: estudo transversal realizado de março a dezembro de 2014 com mulheres provenientes do Serviço de Assistência Especializada (SAE) cadastradas no Sistema de Controle Logístico de Medicamentos (SISCLOM) com diagnóstico de Aids no município de Imperatriz. Foram selecionadas aquelas em TARV há pelo menos seis meses, com 18 anos ou mais, que relataram prática sexual antes do diagnóstico de Aids e capazes de se comunicar. As variáveis sócio demográficas e comportamentais de interesse, fatores clínicos relacionados à presença de comorbidades foram registrados em formulário próprio. A seguir para avaliação do desempenho sexual responderam o questionário Female Sexual Function Index (FSFI). Ambos foram respondidos concomitantemente à coleta de sangue para contagem de linfócitos T, realizada no laboratório do SAE duas vezes por semana. A amostra representativa baseou-se no quantitativo de mulheres cadastradas no SICLOM, com erro amostral de 5%, intervalo de confiança de 95% e valor de alfa ≤ 5%. Foram utilizados os testes Qui-Quadrado para avaliar a associação entre as variáveis, e quando necessário o de Kruskal- Wallis, o teste de Spearman para avaliar a correlação entre CD4/CD8 e FSFI. RESULTADOS: a amostra constou 149 mulheres incluídas, notou-se que as maiores média e mediana do escore do FSFI coincidiram com as maiores médias da contagem de Linfócitos T- CD4 a partir do 2º quartil (Teste de Kruskal Wallis p=0,0347), e houve associação positiva entre FSFI e a relação CD4/CD8 (p=0,0264), confirmando a hipótese alternativa (Correlação de Spearman). CONCLUSÃO: houve associação positiva entre o desempenho sexual ou atividade sexual, com ou sem camisinha, com a contagem de linfócitos T-CD4 e relação CD4/CD8.
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Scully, Ralph. "Mechanisms in transplantation tolerance." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321084.
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Wagner, David H. "Role of the Cd40-cd40 Ligand Interaction in Cd4(+) T Cell Activation of Monocyte Interleukin-1 Synthesis." Digital Commons @ East Tennessee State University, 1994. https://dc.etsu.edu/etd/2816.
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Most studies of the induction of cytokine synthesis in monocytes have used an exogenous triggering agent such as Lipolpoysaccharide (LPS). However, during nonseptic chronic inflammatory responses (e.g., rheumatoid arthritis) monocyte activation occurs as a result of T cell generated signals. This report demonstrated that plasma membranes from anti-CD3 activated peripheral CD4$\sp{+}$ T cells (Tm$\sp{\rm A}$) but not from resting CD4$\sp{+}$ cells (Tm$\sp{\rm R}$) induced monocytes to synthesize IL-1 in the absence of costimulatory cytokines. The expression kinetics of the molecule(s) unique to activated T cells which interact with monocyte receptors to induce IL-1 demonstrated that optimal expression occurred at 6h post activation. This matched Lederman's, et al., (1992) previously reported kinetics of expression of CD40 ligand (CD40L) on activated peripheral T cells, implicating the CD40-CD40L interaction as a candidate for the initiator of IL-1 induction in monocytes. In this work, it was demonstrated that the signal could be reduced up to 85% by addition of 5c8, a monoclonal anti-CD40L antibody. In addition, a monoclonal anti-CD40 IgM (BL-C4) induced resting monocytes to synthesize IL-1. Experiments demonstrated that crosslinking the CD40 molecules on monocytes was critical for IL-1 induction. Tm$\sp{\rm A}$ but not Tm$\sp{\rm R}$ also up-regulated cell surface expression of adhesion/costimulatory molecules on monocytes including CD40, ICAM-1, and LFA-3. Anti-CD40 signaling up-regulated expression of ICAM-1 and LFA-3. Experiments suggested that signaling through CD40 may utilize a protein tyrosine kinase (PTK) mediated pathway but not a protein kinase C mediated pathway and studies using THP-1, a premonocytic cell line, indicated that the transcription factor, NF-$\kappa$B, was activated through anti-CD40 signaling. Since CD40 ligand-transfected cells alone did not induce IL-1 but Tm$\sp{\rm A}$ did, it was considered that an additional costimulatory cell surface molecule was required. Preliminary experiments suggested that CD69 may be required. In summary, these results indicate that contact-dependent T cell-monocyte interactions, alone, can activate inflammatory cytokine production by resting monocytes and that a critical component of this interaction is the CD40-CD40L signaling event.
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Behrendt, Anne [Verfasser], and Reinhard [Akademischer Betreuer] Obst. "Differential antigen dependency of CD4+ and CD8+ T cells / Anne Behrendt. Betreuer: Reinhard Obst." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1055907378/34.
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Maroun, Christiane. "Distinct mechanisms regulate antigen receptor mediated signalling in CD4+ and CD8+ primary T cells." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39960.
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For the last two decades, available results have suggested that CD4 and CD8 are functional analogs which, expressed in a mutually exclusive fashion, have provided a fundamental basis for the characterization of the two T cell lineages. This functional analogy has been described during both T cell development and maturation, as well as during the activation of mature peripheral T lymphocytes. It has been demonstrated that the stringency for CD4/CD8 expression, and their ability to interact with MHC molecules during positive and negative selection, are comparable. Further, mAb mediated coaggregation of either CD4 or CD8 with TCR$ alpha beta$ enhances TCR$ alpha beta$ mediated responses in mature T cells to the same degree. These studies have suggested that both CD4 and CD8 need be juxtaposed with the antigen receptor complex in order to provide their positive functions. We have re-addressed the role of CD4 and CD8 during antigen receptor mediated T cell activation, and have characterized major distinctions between these two accessory activation molecules. Thus, while aggregation of membrane CD4 on primary CD4$ sp+$ lymph node T cells results in a 10-fold inhibition of DNA synthesis subsequently induced through TCR$ alpha beta,$ aggregation of CD8 on CD8$ sp+$ primary T cells has no effect. These results are correlated with the differential localization and activity of Lck in the two T cell lineages. Further, while membrane expression of the tyrosine specific phosphatase, CD45, predicates TCR$ alpha beta$ signalling both in CD4$ sp+$ and CD8$ sp+$ T cells, we present evidence indicating that the mechanism through which this phosphatase functions is distinct in the two T cell lineages. Taken together, the results presented demonstrate fundamental differences in the constraints placed on antigen receptor signalling in the two T cell lineages, which may reflect the distinct properties of CD4 and CD8 themselves, and/or lineage specific differences arising as a consequen