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Thomas, Ian James. "Investigation of the differential effects of CD80 and CD86 costimulation on CD8 T cells." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424069.
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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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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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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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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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Jiang, Janina Q. "The production of HIV suppressive factors by CD28, CD38 and HLA-DR subpopulations of CD8+ T cells." Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9104.
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We have examined CD8+ sub-populations to determine whether these subsets are critical to the production of CD8+ T cell nonlytic factors. The production of the beta-chemokines MIP-1alpha, MIP-1beta and RANTES, and the chemoattractant cytokine IL-16 were measured in cells derived from 24 HIV-infected and 25 uninfected subjects. Asymptomatic HIV+ subjects (CD4 > 200/ul) produced significantly higher levels of MIP-1alpha and MIP-1beta from CD8+ T cells and some sub-phenotypes. Higher RANTES levels were produced by CD28-, CD38- and HLA-DR+/- sub-phenotypes. However, IL-16 was only modulated in the CD38+ subset in comparison to total CD8+ T cells. Infection of CD8+ T cells and sub-populations resulted in generally increased levels of chemokine and IL-16 production, which dissipated over a 15 day time course. Moreover, CD8+ antiviral factor (CAF) activity, another major component of CD8+ T cell nonlytic suppression factors, was not associated with chemokine production. However, significantly higher levels of CAF were produced by CD38+ and HLA-DR+ sub-populations. In addition, we also showed that in CD8+ T cell populations, the production of MIP-1alpha, MIP-1beta and IL-16 was inversely correlated with virus copy number. These findings shed light on the noncytotoxic responses of CD8+ T cells in controlling the natural course of HIV infection.
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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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Potthast, Kerstin. "Interaktion des humanen CD8 mit MHC Klasse I und CD3-TCR." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967744253.
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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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Clement, Mathew. "The role of the CD8 co-receptor in CD8+ T-cell activation." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/47019/.
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CD8+ T-cells are essential for the immune control of pathogens and the natural eradication of cancer. CD8+ T-cells also play a major role in the pathogenesis of autoimmunity and alloreactivity. CD8+ T-cells recognize short peptide fragments (8-13 amino acids) presented at the target cell surface bound to Major Histocompatability Class I (MHCI) molecules. Tcell antigen recognition is unique in nature because it involves the binding of a single ligand (peptide–MHC [pMHC]) by two receptors (TCR and CD8). The CD8 glycoprotein, which serves as the coreceptor on MHCI-restricted T-cells, acts to enhance the antigen sensitivity of T-cells by binding to a largely invariant region of MHCI at a site distinct from the TCR docking platform. CD8 has been shown to have multiple roles including enhancing effects on early T-cell activation events and also in controlling the level of T-cell cross-reactivity. The pMHCI/CD8 interaction is classified as having a very weak binding affinity and very fast kinetics. I discovered that this low solution binding affinity is essential in maintaining homeostasis as dramatically increasing the strength of this interaction resulted in total loss of T-cell specificity and activation independent of TCR engagement. This led me to examine the possibility that anti-CD8 antibodies could also bypass the normal requirements for T-cell activation. I identified one specific clonotype of antibody capable of this phenomenon but simultaneously discovered multiple effector phenotypes of other anti-CD8 antibodies. These included both enhancing and inhibitory effects on pMHCI tetramer binding and CD8+ T-cell activation. Subsequently, I explored the possibility of using these inhibitory anti-CD8 antibodies to block T-cell function in systems which are highly dependent on CD8 such as autoreactive CD8+ T-cells. I demonstrated that targeting CD8 can be used as a strategy to block autoreactive CD8+ T-cell activation in the absence of any effect on pathogen specific immunity. This highlights a novel therapeutic strategy that warrants further investigation. Finally, I demonstrated that CD8 can alter the functional avidity of a CD8+ T-cell for its agonists and act to re-arrange the relative potencies of each of its potential agonists, a novel “focussing mechanism” for CD8 in T cell activation. These results provide new insight to the biological role of CD8 in T-cells and even predict a novel mechanism for CD8 in controlling T-cell function. My results also highlight the potential of targeting CD8 for immunotherapeutic design in autoimmune disorders.
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Arévalo, Suárez Fernando, Sabino Portugal, Carlos Barreda, Pedro Montes, María Teresa Perez-Narrea, Omar Rodríguez, Greys Vergara, and Eduardo Monge. "Enfermedad celíaca vs. atrofia villositaria serológicamente negativa: similitudes y diferencias histológicas y en el perfil inmunohistoquímico de linfocitos CD3, CD4, CD8 y CD56." Sociedad de Gastroenterología del Perú (SGP), 2016. http://hdl.handle.net/10757/617280.
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Existe un grupo de enteropatía conocidas como AVSN que pueden simular enfermedad celíaca. Objetivo: El objetivo de este estudio es describir los hallazgos histológicos y de inmunohistoquímica en pacientes con enfermedad celíaca y AVSN. Material y métodos: 15 biopsias de pacientes con enfermedad celíaca y 19 biopsias con AVSN fueron reexaminados. Se estudió características histológicas tales como atrofia severa, hiperplasia de criptas, número de células plasmáticas, número de eosinófilos y presencia de neutrófilos. Asimismo, a través de inmunohistoquímica se estudió la presencia de linfocitos CD4, CD8, CD3, CD56. Resultados: Se encontró diferencia significativa en la mayor presencia de hiperplasia de criptas (p=0,0348) y mayor número de células plasmáticas (p=0,0348) en las biopsias de enfermedad celíaca que en las catalogadas como AVSN. El número de linfocitos CD8, CD4, CD56 y su distribución fue similar en ambos grupos. El porcentaje de linfocitos intraepiteliales CD3 positivos (p=0,0144) fue mayor en pacientes con AVSN. Conclusión: Los hallazgos histológicos e inmunohistoquímicos muestran más similitudes que diferencias. La diferencia hallada en nuestro estudio sugiere mayor respuesta inmune humoral en pacientes con enfermedad celiaca que en AVSN.There is a group of enteropathies recently known as seronegative villous atrophy (SNVA), which can simulate celiac disease. Objective: The aim of this study was to describe histological and immunohistochemical differences between a group of Celiac disease and SNVA patients. Material and methods: Microscopy reexamination and Immunohistochemistry study were performed for a group of 15 celiac patients and 19 SNVA patients. Histological features as severe atrophy, crypt hyperplasia, plasma cells number, eosinophils number, neutrophils presence were studied; CD4, CD8, CD3, and CD56 markers were studied through immunohistochemistry. Results: There was a significant difference between the frequency of observation of crypt hyperplasia (p=0.0348) and plasma cells (p=0.0348) in celiac disease patients than SNVA patients. In celiac disease was bigger. The number and distribution of CD 8, CD4 and CD56 lymphocytes was similar in both groups. The percentage of CD3 positive intraepithelial lymphocytes (p=0.0144) was higher in SNVA. Conclusion: Histological and immunohistochemical evaluation shows more similarities than differences. The differences found in this study suggest more humoral immune response in celiac disease than in SNVA.
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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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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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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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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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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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Finch, Rosalynde J. "Regulation of interleukin-2 gene transcription in CD8 positive cells /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8352.
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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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Waller, Edward Charles Patrick. "Characterisation of Human Cytomegalovirus-specific CD8+ CD45RA+ CD28- revertant memory T cells (TEMRA)." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612047.
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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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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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Phothirath, Phoukham. "Génération de cellules T CD4+CD25+ suppressives induite par des lymphocytes T CD8+CD28- au cours de réactions leucocytaires mixtes autologues." Lyon 1, 2002. http://www.theses.fr/2002LYO1T195.
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La 4ème de couverture indique : "La réaction mixte lymphocytaire autologue (aMLR) permet l'étude des circuits de régulation du système immunitaire et correspond à la prolifération des lymphocytes T CD4+ suite à une stimulation par des cellules dendritiques autologues (aMLRs déficientes dans: maladie de Hodgkin, syndrome de Down, lupus érythémateux systématique, arthrite rhumatoi͏̈de, cirrhose biliaire primitive, etc). Les lymphocytes T CD8+CD28- sont des cellules régulatrices capables de suppression directe de l'allo- et la xéno-réactivité de lymphocytes T CD4+ et de rendre tolérogènes des cellules dentritiques. L'objectif de notre étude est de développer un système de co-culture in vitro permettant l'étude des rôles suppresseurs des lymphocytes T CD8+CD28-. Ce sont les MLR autologues de 5 jours: (Mo-DCs. Cellules T CD4+. Cellules T CD8+CD28-). Les résultats montrent une forte réponse proliférative des cellules T CD4+, qui est inhibée par des anticorps monoclonaux dirigés contre HLA DR, CD2, CD11a, CD54 et CD86 et s'accompagne d'une sécrétion d'IFN-g et d'IL-12, reflétant une réponse de typeTh1. De plus, on observe l'émergence d'une population cellulaire de phénotype CD4+ CD25+ CTLA4+ (expression intracellulaire et membranaire) CD45RA- 45RO+ au cours de l'aMLR : ces cellules, dotées par ailleurs de faibles capacités prolifératives, sont capables de supprimer par contact cellulaire la réactivité de lymphocytes T CD4+ vis-à-vis d'auto- et d'allo-antigènes présentés par des DCs matures. Notre étude montre que cette population cellulaire T CD8+CD28- pourraitégalement exercer des fonctions régulatrices indirectes en générant une population de lymphocytes T aux fonctions suppressives. Nous montrons donc qu'il est possible de générer in vitro, et dans un modèle syngénique, des lymphocytes T régulatrices CD4+CD25+. S'agit-il ici de lymphocytes générés de novo? Ou alors la MLR autologue a-t-elle permis d'amplifier une population régulatrice existante et quiescente? Ce système pourrait refléter un mécanisme intervenant dans le maintien de la tolérance périphérique, par génération de cellules T régulatrices. "
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Salou, Marion. "Implication des lymphocytes T CD8+ à répertoire restreint dans la sclérose en plaques." Nantes, 2014. http://archive.bu.univ-nantes.fr/pollux/show.action?id=e869cf43-0e5b-473b-a99c-81c495b4b59d.
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La Sclérose En Plaques (SEP) est une maladie autoimmune démyélinisante du Système Nerveux Central (SNC), dans laquelle les lymphocytes T (LT) CD4+ semblent jouer un rôle majeur. L'implication des LT CD8+ a été mise en évidence plus récemment, grâce à de nombreux arguments génétiques, neuropathologiques et immunologiques. Dans des lésions du SNC de patients, les LT CD8+ sont prédominants et ont une répartition oligoclonale, suggérant une infiltration ou une prolifération in situ dépendante d'un antigène. Pour savoir si ces cellules sont accessibles depuis le sang et/ou le liquide céphalorachidien (LCR), nous avons étudié le répertoire lymphocytaire T dans ces différents compartiments. Notre travail montre que le LCR et le sang peuvent être utilisés comme source de LT CD8+ oligoclonaux du SNC. De plus, dans le sang et le SNC, ces cellules présentent des caractéristiques suggérant leur implication dans la maladie. En parallèle, nous avons étudié une nouvelle sous-population de LT innés présentant un récepteur T semi-invariant, les cellules MAIT (Mucosal Associated Invariant T). Ces cellules, qui expriment les marqueurs de cellules productrices d'IL-17, sont importantes dans l'immunité antimicrobienne. Bien que dérégulées en périphérie chez les patients, elles ne semblent pas s'activer différemment des cellules des témoins. Elles sont présentes en faible quantité dans le SNC, en accord avec leur faible capacité de transmigration, et sont susceptibles d'y exercer un rôle non spécifique. En conclusion, ce travail a permis de mieux comprendre l'implication de sous-population de LT CD8+ dans la physiopathologie de la SEPMultiple Sclerosis (MS) is an autoimmune disease of the Central Nervous System (CNS) in which CD4+ T lymphocytes are thought to play pivotal roles. More recently, numerous studies assessing neuropathological, genetic, and immunological parameters have highlighted the importance of CD8+ T cells in the physiopathology of the disease. These cells outnumber CD4+ T cells and have an oligoclonal repartition in the CNS lesions of MS patients, suggesting an antigen-driven infiltration or an in situ proliferation. To decipher whether these cells could be isolated from the blood or the cerebrospinal fluid (CSF), we compared the T cell repertoire in these three compartments. Our work shows that CSF and blood samples could be used as a source of clonally expanded CD8+ T cells found at the lesion sites. In the blood and in the CNS, these cells display characteristics suggesting their involvement in the disease. In parallel, we studied MAIT (Mucosal Associated Invariant T) cells, a subset of innate T lymphocytes with a semi-invariant T cell receptor. These cells express makers of IL-17 producing T cells and have been demonstrated to be important in the antimicrobial immunity. Despite their deregulated phenotype in the blood of MS patients, they display similar activation potential as MAIT cells from controls. They are present at a low frequency in the CNS, consistent with their low transmigration abilities. However, they are likely to exert a bystander role in situ. In conclusion, this work gives new insights into the implication of subsets of CD8+ T cells in the physiopathology of MS
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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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Tiosso, Caio de Faria [UNESP]. "Caracterização da resposta imune celular pela expressão imunoistoquímica de CD4, CD8, CD28, CD152, CD56 e FOXP3 em carcinoma mamário de fêmeas caninas." Universidade Estadual Paulista (UNESP), 2012. http://hdl.handle.net/11449/89004.
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tiosso_cf_me_jabo.pdf: 436744 bytes, checksum: 79836ae4ce26da0a2ba481a0fe57e375 (MD5)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O estudo dos tumores mamários em cadelas revela-se como um excelente modelo para a investigação das neoplasias mamárias em mulheres e tanto no homem quanto nos animais a resposta imune pode interferir no desenvolvimento de neoplasias. Este trabalho teve como objetivo avaliar a eficácia e estimulação do sistema imune celular em tumores mamários de fêmeas caninas por meio da expressão de CD4, CD8, CD4+CD25+ (Foxp3), CD28, CD152 e CD56 (NK). A avaliação da expressão desses marcadores foi avaliada por imunoistoquimica, utilizando-se o método estreptoavidina-biotina-peroxidase. Para a realização desse estudo foram coletadas 20 amostras de tumores mamários de fêmeas caninas e essas divididas de acordo com a classificação histopatológica em 2 grupos: 10 carcinomas simples e 10 carcinomas complexos. Em relação aos resultados não se observou diferenças quanto à quantificação das células imunomarcadas quando comparadas segundo o tipo tumoral. No caso dos carcinomas simples evidenciou-se diferença entre a quantificação das células imunomarcadas (P< 0,05) pelo anticorpo CD28 (p=0,03) e Foxp3 (p=0,01) sendo menores que todas as demais marcações. Já para os carcinomas complexos houve diferença entre a quantificação das células imunomarcadas (P= 0,05) pelo anticorpo CD-152 que apresentou valor maior que as demais marcações com exceção do CD8. Os marcadores CD28, CD56 e Foxp3 foram menores que o CD8 (p=0,01) sendo o Foxp3 menor que todos os outros marcadores. No presente estudo observou-se que existe um controle negativo do sistema imune em ambos os casos, porém esse controle negativo foi mais evidente no carcinoma complexo
The mammary tumor study in female dogs is revealed as an excellent model for the investigation of breast tumors in humans. On both species, the immune system can interfere on neoplasia progression. The aim of this study was to evaluate the immunolocalization and quantification of CD4, CD8, CD4+CD25+ (Foxp3), CD28, CD152 and NK in tumour lymphocyte infiltration, to evaluate the efficacy of stimulation and immune system defense in canine mammary carcinoma. The expression of these markers using immunohistochemistry was made by streptoavidin-biotin peroxidase method. The tissues were collected from twenty mammary carcinomas, subdivided in ten simple carcinomas and ten complex carcinomas of twenty female dogs. This study identified no significant differences on quantification of positive cellular staining in simple carcinoma compared with complex carcinoma. The samples of simple carcinoma resulted significant differences on positive staining between the antibodies CD28 (p=0,03) and Foxp3 (p=0,01) and these markers revealed less quantitative staining compared with the others markers (CD4, CD8, CD152 and NK). The samples of complex carcinoma resulted significant differences on cellular staining quantification by the antibody CD152 (p<0,05) compared with the others markers (CD4, Foxp3, CD28, and NK) with exception when compared with CD8. The immune quantification of positive cellular staining about the markers CD28, CD56 and Foxp3 were smaller than CD8 (p=0,01), and the Foxp3 was smallest than those others markers. It was concluded that exist a negative control of immune system to complex and simple mammary carcinoma, but, this negative control was more significant in female dogs with complex mammary carcinoma
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Tiosso, Caio de Faria. "Caracterização da resposta imune celular pela expressão imunoistoquímica de CD4, CD8, CD28, CD152, CD56 e FOXP3 em carcinoma mamário de fêmeas caninas /." Jaboticabal, 2012. http://hdl.handle.net/11449/89004.
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Orientador: Wilter Ricardo Russiano VicenteBanca: Maricy Apparicio Ferreira
Banca: Marcela Marcondes Pinto Rodrigues
Resumo: O estudo dos tumores mamários em cadelas revela-se como um excelente modelo para a investigação das neoplasias mamárias em mulheres e tanto no homem quanto nos animais a resposta imune pode interferir no desenvolvimento de neoplasias. Este trabalho teve como objetivo avaliar a eficácia e estimulação do sistema imune celular em tumores mamários de fêmeas caninas por meio da expressão de CD4, CD8, CD4+CD25+ (Foxp3), CD28, CD152 e CD56 (NK). A avaliação da expressão desses marcadores foi avaliada por imunoistoquimica, utilizando-se o método estreptoavidina-biotina-peroxidase. Para a realização desse estudo foram coletadas 20 amostras de tumores mamários de fêmeas caninas e essas divididas de acordo com a classificação histopatológica em 2 grupos: 10 carcinomas simples e 10 carcinomas complexos. Em relação aos resultados não se observou diferenças quanto à quantificação das células imunomarcadas quando comparadas segundo o tipo tumoral. No caso dos carcinomas simples evidenciou-se diferença entre a quantificação das células imunomarcadas (P< 0,05) pelo anticorpo CD28 (p=0,03) e Foxp3 (p=0,01) sendo menores que todas as demais marcações. Já para os carcinomas complexos houve diferença entre a quantificação das células imunomarcadas (P= 0,05) pelo anticorpo CD-152 que apresentou valor maior que as demais marcações com exceção do CD8. Os marcadores CD28, CD56 e Foxp3 foram menores que o CD8 (p=0,01) sendo o Foxp3 menor que todos os outros marcadores. No presente estudo observou-se que existe um controle negativo do sistema imune em ambos os casos, porém esse controle negativo foi mais evidente no carcinoma complexo
Abstract: The mammary tumor study in female dogs is revealed as an excellent model for the investigation of breast tumors in humans. On both species, the immune system can interfere on neoplasia progression. The aim of this study was to evaluate the immunolocalization and quantification of CD4, CD8, CD4+CD25+ (Foxp3), CD28, CD152 and NK in tumour lymphocyte infiltration, to evaluate the efficacy of stimulation and immune system defense in canine mammary carcinoma. The expression of these markers using immunohistochemistry was made by streptoavidin-biotin peroxidase method. The tissues were collected from twenty mammary carcinomas, subdivided in ten simple carcinomas and ten complex carcinomas of twenty female dogs. This study identified no significant differences on quantification of positive cellular staining in simple carcinoma compared with complex carcinoma. The samples of simple carcinoma resulted significant differences on positive staining between the antibodies CD28 (p=0,03) and Foxp3 (p=0,01) and these markers revealed less quantitative staining compared with the others markers (CD4, CD8, CD152 and NK). The samples of complex carcinoma resulted significant differences on cellular staining quantification by the antibody CD152 (p<0,05) compared with the others markers (CD4, Foxp3, CD28, and NK) with exception when compared with CD8. The immune quantification of positive cellular staining about the markers CD28, CD56 and Foxp3 were smaller than CD8 (p=0,01), and the Foxp3 was smallest than those others markers. It was concluded that exist a negative control of immune system to complex and simple mammary carcinoma, but, this negative control was more significant in female dogs with complex mammary carcinoma
Mestre
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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
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English, Kieran. "Deciphering the cellular mechanisms promoting CD4+ T cell-dependent intrahepatic CD8+ T cell immunity." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/27735.
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The liver is the body’s largest internal organ and assumes many important physiological and metabolic functions. It is also well-established that the liver possesses unique immunological properties and a delicate balance between tolerance and immunity exists within this large organ. CD4 T cell help to CD8 T cells has emerged as a critical factor involved in promoting robust CD8 T cell responses against viral and tumour antigens. Studies in humans and chimpanzees indicate that CD4 T cells are critical for strong intrahepatic CD8 T cell responses and the spontaneous control of hepatitis C virus and hepatitis B virus infections. However, due to limitations of current small animal models, the precise role of CD4 help in orchestrating intrahepatic CD8 T cell responses, and the mechanisms by which CD4 help is transferred to intrahepatic CD8 T cells remains poorly understood. Using an rAAV based approach to express model antigens containing both CD4 and CD8 T cell epitopes specifically in hepatocytes, we first demonstrate that CD4 help enhances the primary expansion of CD8 T cells responding to hepatocyte expressed antigens, which is critical for the generation of a large pool of memory CD8 T cells in the liver, blood and lymphoid tissues. Importantly, we decipher a novel mechanism facilitating the transfer of CD4 help to intrahepatic CD8 T cells: cognate CD40-CD40L licensing of hepatic XCR1 cDC1s in situ within portal tracts and central veins. In deciphering this mechanism, we also uncovered a previously unrecognised interconnected myeloid cell network contained within portal tracts in the steady state and following antigen expression in the liver. Together, these discoveries yield important insights into the mechanisms governing the outcome of intrahepatic immune responses, and suggest avenues for future work, with the possibility of translational research to explore novel therapies to manipulate intrahepatic immunity and hence beneficially alter outcomes in human liver diseases.
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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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Hambor, John Edward. "Bifunctionality of the human CD8 molecule." Case Western Reserve University School of Graduate Studies / OhioLINK, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=case1054916413.
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Sepulveda, Homero. "Activation requirements for CD8 T cells /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9907780.
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Mossu, Adrien. "Régulation de la survie des cellules dendritiques plasmacytoïdes dans un contexte inflammatoire non viral." Thesis, Besançon, 2015. http://www.theses.fr/2015BESA3011/document.
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Les cellules dendritiques plasmacytoïdes (pDC) sont spécialisées dans la lutte antivirale, notamment grâce à leur capacité à sécréter des IFN de type I. Néanmoins, elles sont aussi impliquées dans Pactivation des réponses immunitaires adaptatives, et des lymphocytes T (LT) en particulier. C'est pourquoi, lors d'épisodes inflammatoires chroniques ou incontrôlés, les pDC sont à l'origine de l'initiation ou du maintien de syndromes inflammatoires et du développement de pathologies auto-immunes. Il doit donc exister des mécanismes permettant de contrôler l'activité de ces cellules. À l'aide d'un modèle in vivo d'inflammation non virale induite par l'injection d'un anticorps anti-CD3 (Ac aCD3), nous avons observé une apoptose des pDC dans différents organes lymphoïdes, et ce de façon dépendante de l'activation des lymphocytes T. De plus, nous avons pu observer que la diminution de la survie des pDC dans ce contexte inflammatoire n'était pas associée à l'orage cytokinique induit par l'efièt mitogénique de l'Ac aCD3. En revanche nos résultats montrent que les LT CD8* et la voie cytotoxique de la perforine dans ce contexte inflammatoire aigu sont responsables de la déplétion des pDC. Nous avons également étendu ces résultats à d'autres situations inflammatoires stériles comme lors de la maladie du greffon contre l'hôte. Ces données suggèrent que cette voie de régulation pourrait être utilisée à des fins thérapeutiques, afin de contrôler la survie des pDC impliquées dans la physiopathologie de syndromes auto-immuns comme le lupus érythémateux disséminé, le psoriasis, la sclérose en plaques ou encore le diabète de type IPlasmacytoid dendritic cells (pDC) are specialized in type I interferons (IFN-I) secretion to control viral infections. However, these cells can also activate adaptive immune responses, and polarize T cells. Indeed, during chronic or uncontrolled inflammatory episodes, pDC can induce or maintain inflammatory syndromes and autoimmune diseases. So some mechanisms should exist to control the fonction of these cells. In an in vivo modcl of non viral inflammation induced by the injection a CD3-specific antibody (aCD3 Ab), we could observed pDC's apoptosis dependent of T cell activation in different lymphoid organs. Moreover, we could observe that this depletion of pDC was not associated with the cytokinic storm induced by the mitogenic effect after aCD3 Ab treatment. On the other hand our data shovved that CD8+ T cells and the perforin pathway in this acute inflammatory context are responsible for pDC depletion We also obtained the same results in other non viral inflammation settings such as graft versus host disease. Overall, these data suggesi that this regulation pathway could be used for therapeutic purposes, to control pDC survival and avoid their involvement in the physiopathology of autoimmune disorders like systemic lupus erythematosus, psoriasis, multiple sclerosis or type I diabetes
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Daniel, Alexandre Gonçalves Teixeira. "Avaliação dos níveis de linfócitos T CD4+, T CD8+ e da razão CD4+/CD8+ em gatos da raça Maine Coon com gengivite crônica e infectados ou não pelo Herpesvírus tipo 1 e/ou calicivírus." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-03082012-163218/.
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Sabe-se que um dos principais problemas odontológicos na clínica de felinos é a gengivite crônica e intratável. Tal afecção pode ser iniciada e/ou exacerbada por agentes virais, como o vírus da imunodeficiência dos felinos (FIV), o Herpesvírus tipo 1 e o Calicivírus. Os gatos da raça Maine Coon apresentam grande predisposição ao desenvolvimento de gengivite-estomatite juvenil e intratável. A depleção de linfócitos T CD4+ e T CD8+ pode exercer papel determinante na iniciação e manutenção das doenças inflamatórias da gengiva. O escopo do presente estudo foi verificar se os animais da raça Maine Coon são mais predispostos à calicivirose, bem como avaliar quantitativamente a resposta imunológica celular, mediada por linfócitos TCD4+ e TCD8+, visando a correlacionar à influência do número de linfócitos na presença e curso da gengivite nesta determinada raça, utilizando-se como controle gatos de outras raças com e sem gengivite. Os valores absolutos médios de linfócitos totais em Maine Coons com gengivite crônica mostraram-se inferiores aos de gatos da raça Maine Coon sem doença oral e de gatos de outras raças com gengivite crônica (p<0,05); os valores médios de linfócitos TCD4+ em Maine Coons com gengivite crônica mostraram-se inferiores quando comparados aos valores de animais da mesma raça, sem doença oral instalada (p<0,05); animais da raça Maine Coon possuem menor relação CD4+:CD8+ quando comparados a animais de outras raças com gengivite crônica e também quando comparados a Maine Coons sem doença oral (p<0,05). O calicivírus está altamente relacionado à ocorrência da gengivite, independentemente da raça estudada, não havendo maior prevalência na raça Maine Coon. O efeito do calicivírus não foi significativo nas alterações de nenhuma das variáveis celulares estudadas. Tais fatos apontam para uma possível predisposição racial ao quadroinflamatório gengival, com alteração de alguns componentes celulares relacionados à imunidade celular. Isto tem como fator importante alertar o clínico frente ao uso de glicocorticóides no tratamento da gengivite crônica nesta raça, visando a evitar maior comprometimento da imunidade celular destes animais.Chronic untreatable feline gingivitis is widely recognized as one of the major oral diseases seen in feline patients. It can be either triggered or exacerbated by virus such as feline immunodeficiency virus, feline herpesvirus type 1 and calicivirus. One may therefore propose that lymphocytes T CD4+ and T CD8+ depletion can play an important role in initiating and maintaining the inflammatory gingival disease. Maine Coon cats are highly predisposed to juvenile untreatable gingivitis. The purpose of this study was to evaluate whether Maine Coon cats are more predisposed to calicivirus infection and to verify, quantitatively, their immunological cellular response mediated by lymphocytes T CD4+ and TCD8+. The main idea was to investigate the influence imposed by lymphocyte counts in gingivitis development and progression within this breed; for this, we selected non-Maine Coon cats (with and without gingivitis) to serve as controls. Mean absolute values of total lymphocytes in Maine Coon cats presented with gingivitis were inferior than the same values taken for both Maine Coon cats free of oral disease and non-Maine Coon cats with chronic gingivitis (p<0,05); lymphocytes TCD4+ average values in Maine Coon cats with chronic gingivitis were also lower than the ones taken from cats of the same breed but without oral disease (p<0,05). Maine Coon cats have lower CD4+:CD8+ ratio when compared to non-Maine Coon cats with chronic gingivitis as well as with Maine Coon cats without oral disease (p<0,05). The calicivirus is highly involved with the occurrence of gingivitis, no matter the breed being evaluated. The action virus imposes in changing cellular immunology was not significant, at least considering the cellular variables studied. All these lead us to point out a possible breed predisposition to the gingival inflammation, with modification of some cellular components related with cellular immunity. Furthermore, concerning practical terms, these results serve as a relevant alert to the clinicians regarding the use of glucocorticoids for treating chronic gingivitis in this breed, in order to prevent further impairment of cellular immunity of these animals.