Dissertations / Theses: 'Naine T'

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Ferreira, Cristina da ConceicÌ§aÌƒo Varandas. "Naive T cell survival : analysis of transgenic monoclonal T cell populations." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250701.

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Yang, Liang Peng. "The maturation of naive human CD4 T lymphocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq21528.pdf.

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Gaß, Nadine [Verfasser], and H. A. [Akademischer Betreuer] Wagenknecht. "PhotoDNAzyme - Asymmetrische Katalyse und Distanzabhängigkeit der T-T-Dimerbildung / Nadine Gaß ; Betreuer: H.-A. Wagenknecht." Karlsruhe : KIT-Bibliothek, 2016. http://d-nb.info/1122461518/34.

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Grebe, Nadine [Verfasser]. "Analyse humaner regulatorischer T-Zellen im humanisierten Mausmodell / Nadine Grebe." Mainz : Universitätsbibliothek Mainz, 2013. http://d-nb.info/103701264X/34.

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Cowan, Teresa. "The TCRBJ and TCRBV repertoire in naive and memory human T-cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34173.pdf.

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Martin, Matthew David. "Naive and memory CD8 T cell responses after antigen stimulation in vivo." Thesis, University of Iowa, 2011. https://ir.uiowa.edu/etd/1246.

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The extent to which the progeny of one primary memory CD8 T cell differs from the progeny of one naïve CD8 T cell of the same specificity remains an important question. In order to explore cell autonomous functional differences between naïve and memory CD8 T cells that are not influenced by differences in the priming environment, an experimental model has been developed in which physiological numbers of both populations of cells were co-transferred into naïve host before antigen-stimulation. Interestingly, naïve CD8 T cells expand in numbers more than primary memory CD8 T cells after various infections or immunizations. The intrinsic ability of one naïve CD8 T cell to give rise to more effector CD8 T cells than one memory CD8 T cell is independent of the number of primary memory CD8 T cells present in vivo. The sustained proliferation of primary, but not the increased death of secondary effectors was shown to contribute to the differences in the observed magnitudes of expansion. In addition, longitudinal analysis of primary and secondary CD8 T cell responses revealed that the ability of naïve CD8 T cells to generate long-lived progeny (`memory generation potential') is better than for primary memory CD8 T cells despite the differences in overall kinetics of both responses after infection. Taken together, the data presented here revealed previously unappreciated differences between naïve and memory CD8 T cells and will help further define the functional potential for both cell types. The goal of immunization is to generate memory CD8 T cells of sufficient quality and quantity, and it has been shown that the naïve to primary memory CD8 T cell differentiation in vivo is controlled, at least in part, by the amount and duration of inflammation present early after the initiation of the response. In experiments where naïve CD8 T cells were co-transferred with increasing numbers of primary memory CD8 T cells, we observed a negative correlation between the number of primary memory present and the magnitude of primary CD8 T cell responses. Interestingly, the conversion of newly recruited (either TCR-Tg or endogenous) primary CD8 T cells into CD8 T cells with the phenotype (CD62Lhi, CD27hi) and function (tissue distribution, Ag-driven proliferation, cytokine production) of long-term memory was facilitated when they were primed in the presence of memory CD8 T cells of the same or unrelated specificity. Therefore, these data suggest that the presence of anti-vectorial immunity will not necessarily decrease the efficacy of CD8 T cell vaccination since newly recruited CD8 T cells, despite their decreased magnitude of expansion, might differentiate into functional memory cells faster.

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Yang, Edward. "The localization of naive and memory CD8⁺ T cells following infection." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1465089.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed June 22, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 43-45).

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Correia, Rodolfo Patussi. "Estudo da distribuição de células T naive e subtipos de células T de memória em neoplasias hematológicas." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-19042013-092628/.

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Células T de memória são a marca registrada da imunidade adaptativa, e podem ser caracterizadas em central memory (TCM) e effector memory (TEM) T cells. A participação destas células no curso de doenças hematológicas é descrita como mecanismo relacionado à evolução das mesmas. Neste trabalho, analisamos o sangue periférico de doadores de sangue e pacientes com Mielodisplasia (SMD), Mieloma Múltiplo (MM) e Leucemia linfocítica crônica B (LLC), e avaliamos a distribuição das células T CD4+ e CD8+ naive e de memória. SMD e MM não apresentaram resultados significativos, mas na LLC, as células T CD4+ estavam alteradas e dependentes do prognóstico, com aumento das células TCM somente nos pacientes com prognóstico ruim. Essas evidências sugerem que interações imunológicas entre células B da LLC e células T CD4+ possa ser um mecanismo próprio da doença que venha interferir na fisiopatologia e favorecer a geração de células TCM, que podem fornecer sinais de sobrevivência, como citocinas e CD40L, contribuindo assim para o estabelecimento e agressividade da LLC.
Memory T cells are the hallmark of adaptive immunity and are characterized as central (TCM) and effector memory (TEM) T cells. The influence of T cells in the course of hematological malignancies has been described as a mechanism related to the evolution. In this study, we analyzed the peripheral blood of healthy donors and patients with myelodysplastic syndrome (MDS), multiple myeloma (MM) and chronic lymphocytic leukemia B (CLL), and analyzed the distribution of CD4+ and CD8+ naive and memory T cells. MDS and MM revealed no significant difference, but CLL patients showed changes in CD4+ T cell and it were dependent on the prognosis. Patients with poor prognosis presented increased in frequency and absolute number of TCM cells. These evidences show that immunological interactions between CLL and CD4+ T cells could be a disease mechanism that could interfere in pathophysiology and result in the generation of TCM cells, that provide survival signals to the tumor clone, such as cytokines and CD40L, thus contributing to establishment and more aggressive CLL progression.

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Hoellman, John Richard. "Contact-Dependent Activation of Macrophages by Naive CD4⁺ T cells." [Johnson City, Tenn. : East Tennessee State University], 2000. http://etd-submit.etsu.edu/etd/theses/available/etd-0602100-130806/restricted/electhesisJU21c.pdf.

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Stirk, Emily Ruth. "Stochastic modelling of diversity and ageing in the naive T cell repertoire." Thesis, University of Leeds, 2010. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531516.

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Ali, Taccyanna Mikulski. "Perfil de expressão de genes da via Wnt/beta-catenina em timócitos e linfócitos T CD4+ de camundongos BALB/c." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-06112015-144437/.

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INTRODUÇÃO: A molécula HIG2 pode atuar como agonista da via Wnt/beta-catenina, pois se liga ao receptor Frizzled 10 e induz a expressão de genes da mesma. Dados recentes do nosso grupo mostraram expressão diferencial do gene HIG2 em células mononucleares do sangue periférico e em especial linfócitos T CD4+ naïve, mas não em células diferenciadas de memória em indivíduos sadios. Também observamos in vitro em linfócitos T CD4+ de indivíduos saudáveis que o peptídeo sintético HIG2 induziu a ativação da via Wnt/beta-catenina, produção de HIG2 e outros produtos da via, além da proliferação de células T CD4+ naïve sugerindo um papel do HIG2 na proliferação homeostática de linfócitos T CD4+. HIPÓTESE: Como as células T CD4+ naïve são diretamente exportadas pelo timo, os níveis aumentados de HIG2 neste tipo celular sejam decorrentes da ativação da via Wnt/?-catenina nos estágios tardios da diferenciação de timócitos. Portanto, as células T CD4+ naïve e timócitos simples positivos para CD4 (SP CD4) apresentariam perfil semelhante de expressão de HIG2 e genes da via Wnt/beta-catenina, incluindo receptores, fatores de transcrição, genes estruturais da via e alvos quando comparadas as demais populações celulares. OBJETIVO: Avaliar a expressão de HIG2 e outros genes da via Wnt/beta-catenina em timócitos e linfócitos T CD4+ naïve e memória de camundongos. MÉTODOS: Isolamos timócitos duplo negativos (DN), timócitos duplo positivos (DP), simples positivos para CD4 e CD8 (SP CD4 e SP CD8) de timo e também células T CD4+ naïve e memória do baço dos mesmos camundongos pelo procedimento de citometria de fluxo. Analisamos a expressão de vários genes da via Wnt/beta-catenina por PCR em tempo real. RESULTADOS: Em timócitos DN há expressão significativa dos genes que codificam para Frizzled 6, LRP5, TCF-1 e TCF-4 em relação as outras populações celulares. Nos timócitos DP há maior expressão dos genes que codificam para LRP5, LRP6, beta-catenina, GSK-3beta, TCF-1 e Bcl-XL em relação às demais populações. Em timócitos SP CD4 foi detectada expressão diferencial de genes que codificam para Frizzled 10, LRP6, beta-catenina, LEF-1 e HIG2 enquanto que na população de timócitos SP CD8 não observamos expressão significativa de nenhum gene da via Wnt/beta-catenina. Nas células T CD4+ naïve há expressão significativa de Frizzled 5 e Frizzled 10 quando comparadas a timócitos SP CD8 e células T CD4+ de memória . Já nos linfócitos T CD4+ de memória, detectamos maior expressão de Frizzled 6, TCF-4, Bcl-XL e ciclina D1 em relação as demais populações. CONCLUSÃO: Cada população apresenta um perfil distinto de expressão gênica. As maiores semelhanças ocorrem entre os timócitos DN e DP onde as principais diferenças são a expressão de Frizzled 6 e Ciclina D1.Os timócitos SP CD4 e as células T CD4+ naïve não apresentaram níveis semelhantes de expressão gênica de elementos da via Wnt canônica, o que não corrobora a hipótese de que o perfil transcripcional de timócitos SP CD4 e linfócitos T CD4+ naïve é semelhante. Ainda, não observamos expressão aumentada de HIG2 em linfócitos T CD4+ naïve comparados aos de memória, o que contrasta com os resultados obtidos anteriormente por nosso grupo com amostras humanas sugerindo que camundongos não regulam a expressão de HIG2 em linfócitos T CD4+ como os seres humanos
INTRODUCTION: HIG2 molecule can act as an agonist of Wnt/?-catenin pathway, because it able to bind to Frizzled 10 receptor and induce the expression of the genes related to this pathway. Recent data from our group have shown differential expression of the HIG2 gene in peripheral blood mononuclear cells, and particularly in naive CD4 + T cells, but not in memory T cells in healthy individuals. We have also observed that inducing the CD4 + T lymphocytes from healthy individuals with HIG2 synthetic peptide in vitro, led to the activation of Wnt/beta-catenin pathway, HIG2 production and expression of other target genes of this pathway and the proliferation of naïve CD4 + T cells, suggesting that HIG2 may play a role in homeostatic proliferation of CD4+ T cells. HYPOTHESIS: As naïve CD4 + T cells are directly exported from the thymus, we have hypothesized that increased levels of HIG2 in this cell type is due to the activation of Wnt/beta-catenin pathway in the later stages of thymocyte differentiation. Therefore, naïve CD4 + T cells and CD4 single-positive thymocytes (CD4 SP) may share a similar pattern of gene expression of HIG2 and Wnt/beta-catenin genes (genes that encodes receptors and co-receptors, transcription factors, structural and target genes) when compared to other cell populations. AIM: our major aim is to evaluate the expression of HIG2 and other genes of the Wnt/beta-catenin in thymocytes, naïve CD4 + T lymphocytes and memory CD4+ T cells from mice. METHODS: We have isolated thymocytes double negative (DN) T cells, positive double positive (DP) T cells, CD4 and CD8 single-positive thymocytes (CD4 SP and CD8 SP) of thymus from BALB/c mice and we have also isolated naïve CD4 + T cells and memory CD4+ T cells of the spleen from the same mice we have used the thymus. We have analysed the expression of several genes of Wnt/beta-catenin by real time PCR RESULTS: In DN cells there was expression of the Frizzled 6, LRP5, TCF-1 and TCF-4 genes compared to other cell populations. In DP thymocytes it could be observed a greater expression of LRP5, LRP6, beta-catenin, GSK-3beta, TCF-1 and Bcl-XL genes compared to other populations. In CD4 SP thymocytes, it was detected differential expression of the Frizzled 10, LRP6, beta-catenin, LEF-1 HIG2 genes and in CD8 SP cells we could not observe significant expression of any gene of Wnt/?-catenin pathway. In naïve CD4 + T cells there was a significant expression of Frizzled5 and Frizzled 10 genes when compared to all the samples. In memory CD4 + T cells, we have detected higher expression of Frizzled 6, TCF-4, Bcl-XL and cyclin D1 genes than in any other populations. CONCLUSION: Each population has a distinct gene expression pattern. The biggest similarities occur between DN and DP thymocytes where the main differences are the expression of Frizzled 6 and cyclin D1.However, the pattern of gene expression in SP thymocytes is not similar to those presented by naïve CD4+ T cells. Moreover, we have not observed increased expression of HIG2 in naïve CD4 + lymphocytes compared to memory CD4+ T cells, which contrasts the results obtained previously by our group with human samples suggesting that mice might not regulate the HIG2 expression in CD4 + T lymphocytes as human beings do

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Brookman-Amissah, Sabine. "Untersuchung der Interaktionskinetik naiver humaner T-Zellen und dendritischer Zellen in dreidimensionaler Kollagenmatrix und Erfassung der T-Zell-Aktivierung und -Proliferation unter Oxidative Mitogenese-Bedingungen." Doctoral thesis, kostenfrei, 2007. http://nbn-resolving.de/urn/resolver.pl?urn=nbn:de:bvb:20-opus-27742.

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Goldrath, Ananda W. "T cell homeostasis : a role for specific peptide/MHC ligands in homeostasis driven proliferation of naive CD8⁺ T cells /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8332.

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Fitz-Gerald, Leslie. "Naive CD4+ T-cell homeostasis in primary progressive and secondary progressive multiple sclerosis." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106368.

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The peripheral naive CD4+ T-cell pool is maintained through homeostatic mechanisms, which balance thymic output, cell survival and death, and peripheral T-cell proliferative processes. Naive CD4+ T-cells are divisible into several subsets based on their surface expression of CD31: cells having highest levels of expression of CD31 correspond to recent thymic emigrants (CD4+ RTEs), whereas CD31-negative (CD31neg) naive CD4+ T-cells have lost CD31 expression and are distant in origin from the thymus. We report that SPMS patients have altered naive CD4+ T-cell homeostasis with increased TCR-signalling and loss of CD31 from naive CD4+ T-cells with increasing age. Second, we report increased proliferation of the CD31neg subset of naive CD4+ T-cells in both SPMS and PPMS compared to controls. PPMS patients had an increased frequency of CD31neg naive CD4+ T-cells expressing the Fas receptor CD95. We conclude in PPMS that CD31neg cells have an increased propensity for cell death following proliferation. Self-peptide-MHC induced TCR signalling helps maintain naive CD4+ T-cell survival. TCR signalling with loss of CD31 leads to loss of the immunoregulatory function of CD31 molecules in naive CD4+ T-cells, i.e. would favour the development of autoimmune processes. Furthermore, increased proliferation of CD31neg naive CD4+ T-cells is known to expand auto-reactive T-cells, i.e. may contribute to ongoing autoimmune processes in progressive MS. In conclusion, we report peripheral naive CD4+ T-cell homeostatic alterations in both SPMS and PPMS that have potential implications for ongoing immunopathogenesis of these MS subtypes.
La population des cellules-T CD4+ naïves périphériques est maintenue par des mécanismes homéostatiques qui fonctionnent en balancent la sortie du thymus, la survie et la mort des cellules, et la prolifération périphériques des cellules-T. Les cellules-T naive CD4+ se divisent en plusieurs sous-ensembles en fonction de leur expression de CD31 en surface: Les cellules ayant un plus haut niveau d'expression de CD31 correspondent aux émigrants thymiques récents (CD4+ ETRs), alors que les cellules CD31-négatif (CD31neg) ont perdu l'expression de CD31 et sont éloignées de l'origine du thymus. Nous avons constaté que chez les patients atteints de SPPS, l`homéostasie des lymphocytes-T CD4+ naïves est alterée, et se caractérise par une augmentation de la signalisation des récepteurs des cellules-T (RCT) et par la perte de CD31 des cellules-T CD4 + naïves avec l'âge. Deuxièmement, nous avons constaté une augmentation de la prolifération du sous-ensemble CD31neg des cellules-T CD4+ naïves chez les patients atteints de SPPS et SPPP comparé aux controles. Les patients atteints de SPPP avaient une fréquence accrue dede type CD31neg exprimant le récepteur Fas, CD95. Nous concluons que les cellules CD31neg des patients atteints de SPPP ont une propension accrue à la mort cellulaire après leur prolifération. La signalisation des TCR induite par le complexe auto-peptide-CMH-induit signalisation des TCR permet de maintenir la survie des cellules-T CD4+ naives. Le signalisation des TCR avec un perte de CD31 entraîne la perte des fonctions immunorégulatrices des molécules CD31 dans les cellules-T CD4+ naives ; i.e. favorisant le développement de processus auto-immunitaires. En outre, la prolifération des cellules-T CD4 + naïves de type CD31neg est une cause connue de l'augmentation des cellules-T auto-réactives, c'est-à-dire peuvent contribuer à l'établissement de processus auto-immunitaires dans la SP progressive. En conclusion, nous rapportons des modifications homéostatique périphériques des lymphocytes-T CD4 + naïves dans les deux SPPS et PPPS ayant des implications potentielles pour l'immunopathogènes de ces sous-types de SP.

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Bähr, Nadine [Verfasser]. "Beeinflussung der T-Zell-vermittelten Immunreaktivität durch Clonidin nach kardiochirurgischen Eingriffen / Nadine Bähr." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1022865722/34.

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Chen, Yuling [Verfasser]. "Immunometabolism of inflamm-aging in naive and memory CD4+ T cells / Yuling Chen." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/120204333X/34.

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Ogura(Kato), Aiko. "CXCR3high CD8+ T cells with naive phenotype and high capacity for IFN-γproduction are generated during homeostatic T-cell proliferation." Kyoto University, 2019. http://hdl.handle.net/2433/242369.

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Soares, Maria Godinho Alves Vieira Duarte. "Regulation of human naive and memory T cell populations by apoptosis and replicative senescence." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397795.

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Wiggett, Helen Elizabeth. "Distinct roles for CD28 and OX40 signals in regulating naive and effector CD4 T cells." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408951.

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Webb, Lindsay M. Webb. "Protein Arginine MethylTransferase 5 (PRMT5) Drives Inflammatory T cell Responses and Autoimmunity." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1540137110161319.

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Anis, Mursalin M. "Modulation of naive CD4+ Tcell activation and dendritic cell function in the lungs during pulmonary mycobacterial infection." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1184427168.

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

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

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Engert, Nadine [Verfasser]. "Phenolic acids and antioxidative capacity on ancient wheat namely einkorn (T. monococcum ssp.), emmer (T. turgidum ssp.) and spelt wheat (T. aestivum ssp. spelta) and on germinated bread wheat (T. aestivum ssp. aestivum) / Nadine Engert." Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1063177758/34.

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Matzmohr, Nadine [Verfasser]. "Die Rolle des Notch-Signalweges für die Modulation inflammatorischer T-Zell-Reaktionen / Nadine Matzmohr, geb. Kaßner." Berlin : Freie Universität Berlin, 2010. http://d-nb.info/1024866513/34.

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Zastepa, Evelyn. "Altered naive CD4 T-cell biology defines a progressive Multiple Sclerosis subgroup: gene expression and functional studies." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114451.

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Background: Multiple sclerosis (MS) is an autoimmune-mediated inflammatory and neurodegenerative disease of the central nervous system. Peripheral immune mechanisms drive disease in relapsing-remitting MS (RRMS), whereas the contribution of immune mechanisms to progressive MS, including secondary progressive MS (SPMS) and primary progressive MS (PPMS), is uncertain. Naive CD4 T-cells initiate autoimmune responses. Our objective was to investigate naive CD4 T-cells in patients with progressive MS. Methods: We compared naive CD4 T-cell gene expression profiles of progressive MS patients and healthy controls (HCs) using whole genome microarrays. Key genes and pathways identified from the microarray study were validated by surface protein expression. Potential functional defects in naive CD4 T-cells were explored by assessing response to T-cell receptor (TCR) stimulation, cytokine production, and proliferative potential. Results: Hierarchical clustering, based on the most variably expressed genes among all patients and controls, segregated progressive MS patients from HCs and separated progressive MS patients into two subgroups, which we termed P-1 and P-2. Most differentially expressed genes between P-1 and HCs were upregulated in P-1 and enriched for immune response genes, whereas in P-2 most differentially expressed genes were downregulated compared to HCs. These findings suggest peripheral immune mechanisms are active only in P-1 patients. SPMS patients from subgroup P-1 had a shorter RRMS duration before conversion to SPMS than SPMS patients from subgroup P-2, suggesting P-1 SPMS patients may have a more aggressive/rapid disease course. In-depth pathway analysis, focusing on P-1 SPMS, suggested altered TCR and toll-like receptor (TLR) signalling in naive CD4 T-cells of P-1 SPMS patients. We report a 5 gene T-cell activation transcriptional signature specific for P-1 SPMS patients. Protein expression studies support the microarray findings: 3 of the 5 signature genes (TLR2, TLR4 and CCR1) had higher membrane expression on freshly isolated naive CD4 T-cells from P-1 SPMS vs. P-2 SPMS patients. TCR stimulation for 48h induced significantly higher TLR expression in P-1 SPMS vs. P-2 SPMS and HCs, as well as increased IFN- secretion in P-1 SPMS. Further, we found higher surface expression of co-stimulatory molecules CD28 and CD27 at 24h in P-1 SPMS, which may have permitted a continued response of naive CD4 T-cells to TCR signalling, explaining the sustained linear increase in TLR protein expression in P-1 SPMS patients. P-2 SPMS patients showed increased CD95 surface expression on naive CD4 T-cells and increased IL-10 secretion after 48h stimulation. No difference in proliferative potential of activated naive CD4 T-cells was observed between the groups. Conclusions: Our transcriptional signature identifies for the first time, a sub-population of SPMS patients having rapid RRMS progression, T-cell immune dysregulation and differences in responses to TCR stimulation. These findings reflect the heterogeneity of progressive MS and suggest that a subgroup of SPMS patients with rapid progression may benefit from anti-inflammatory therapies.
Introduction: La sclérose en plaques (SP) est une maladie à médiation des processus auto-immunes, inflammatoires et neurodégénératives du système nerveux central. Les mécanismes immunologiques périphériques entrainent la maladie en SP récurrente-rémittente (SP-RR), tandis que la contribution des mécanismes immunologiques en SP progressive, incluant SP (secondaire progressive) (SP-SP) et SP primaire progressive (SP-PP), est incertaine. Les cellules T naïves CD4 initient les réponses auto-immunes. Notre objectif était d'étudier les cellules T naïves CD4 en patients atteints de SP progressive. Méthodes: Nous avons comparé les profils d'expression génétiques des lymphocytes T naïves CD4 de patients atteints de SP progressive et les contrôles en utilisant les microarrays du génome complet. Les gènes et voies d'intérêt identifiés de l'étude microarray étaient validés par l'expression de surface des protéines. Des défauts de fonctionnement potentiels des cellules T naives CD4 ont été explorés par l'évaluation de la réponse à signalisation des récepteurs cellules-T (RCT), la production des cytokines, et potentiel prolifératif. Résultats: Regroupement hiérarchique, fondé sur les gènes les plus variablement exprimés parmi tous les patients et contrôles, a ségrégué les patients atteints de SP progressive des contrôles et a séparé les patients atteints de SP progressive en deux sous-groupes, que nous avons appelée P-1 et P-2. Les gènes exprimés de façon différentielle entre P-1 et contrôle étaient régulés à la hausse en P-1 et enrichis des gènes de réponse immunitaire, tandis qu'en P-2 les gènes exprimés de façon différentielle étaient réprimées. Ces résultats suggèrent que les mécanismes immunologiques sont actifs seulement dans les patients de P-1. Les patients SP-SP de sous-groupe P-1 avaient une plus courte durée SP-RR avant la conversion en SP-SP que les patients de SP-SP du sous-groupe P-2, ceci suggérant que les patients de P-1 SP-SP peuvent avoir une évolution de la maladie plus agressive/rapide. L'analyse en profondeur des voies, concentrée sur les patients P-1 SP-SP, suggérait des altérations en signalisation des récepteurs cellules-T (RCT) et des récepteurs de type Toll (RTT) chez les cellules T naives de P-1 SP-SP. Nous rapportons une signature de 5 gènes d'activation des cellules T de la transcription spécifique pour les patients P-1 SP-SP. Des études d'expression de protéines soutiennent les conclusions microarray: 3 des 5 signatures des gènes (TLR2, TLR4, CCR1) avaient d'expression membranaire en hausse sur les cellules T naïves CD4 fraîchement isolées des patients P-1 SP-SP vs. P-2 SP-SP. Stimulation du RCT pour une durée de 48 heures induite de manière significative une augmentation de l'expression de RTT en P-1 SP-SP vs. P-2 SP-SP et contrôles, ainsi qu'une augmentation de production de IFN-γ. En outre, nous avons trouvé une augmentation en expression de surface des molécules de co-stimulation CD28 et CD27 à 24h en P-1 SP-SP, qui peuvent avoir permis une réponse continue de cellules T naïves à signalisation RTT, expliquant l'augmentation soutenue linéaire de l'expression de protéine TRR en patients P-1 SP-SP. Les patients de P-2 SP-SP ont montré une expression membranaire augmentée de CD95 chez les cellules T naives et à augmenté la sécrétion d'IL-10 après de la stimulation pour 48hr. Aucune différence en potentiel prolifératif chez les cellules T naives activées a été observée entre les groupes. Conclusion: Notre signature transcriptionnelle identifie pour la première fois, une sous-population des patients SP-SP ayant une progression rapide de SP-RR, une dysrégulation immunitaire de cellule-T et de différentes réponses à la signalisation des RCT. Ces résultats reflètent l'hétérogénéité de SP progressive et suggèrent qu'un sous-groupe des patients atteints de SP-SP ayant progression rapide peuvent bénéficier du traitement avec thérapies anti-inflammatoires.

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Ali, Ramadan. "NAADP-Mediated Calcium Release in Mammalian Cells: Regulation of Naive and Effector T Cell Functions by NAADP." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1415826878.

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Dubois, Stéphanie. "Cytokine priming enables triggering of naive auto-reactive CD8[superscript +]T cells by weak agonist ligands of the TCR." Mémoire, Université de Sherbrooke, 2010. http://hdl.handle.net/11143/5956.

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Résumé : L'activation des lymphocytes T CD8+ naïfs par un antigène nécessite deux signaux. Le premier signal est médié par le récepteur des cellules T (TCR) à la suite de son interaction avec le complexe majeur d'histocompatibilite (CMH) de classe I. Le deuxième signal est délivré par l'interaction des molécules de co-stimulation avec leur récepteur spécifique retrouvé sur les cellules présentatrices d'antigène professionnelles. Toutefois en réponse à la pression homéostatique, comme dans le cas de la lymphopénie, les lymphocytes T naïfs sont soumis à une prolifération sans stimulation antigénique par un processus appelé «prolifération induite par la lymphopénie (LIP)». LIP des lymphocytes T CD8+ naïfs nécessite IL-7, et un peptide du soi présenté pas le CMH de classe I. Des travaux récents de notre laboratoire ont montré que les cytokines homéostatiques IL-7 et IL-15 peuvent agir en synergie avec IL-21 et induire une prolifération antigène-indépendante des cellules CD8+ naives. Cette activation "sensibilise" les cellules à proliférer en réponse à une concentration sub-optimale de l'antigène spécifique au TCR. Également les cellules pré-stimulées avec des cytokines produisent davantage de cytokines effectrices telles que le TNFa et l'IFNy; et possèdent un potentiel plus élevé de cytotoxicity après stimulation avec un antigène spécifique. Dans mon projet de maitrise, j'ai étudié la possibilité que la pré-stimulation par les cytokines pouvait être un mécanisme important par lequel des cellules T CD8+ naïves qui sont potentiellement autoréactives soient stimulées pour provoquer une maladie auto-immune telle que le diabète de type 1. J'ai démontré cela en utilisant un modèle de souris transgéniques. Ces souris produisent des cellules T CD8+ qui expriment le TCR transgénique P14 (cellules PI4) , lesquelles reconnaissent un peptide antigénique dérivé de l'antigène glycoprotein (GP33) du virus de la chorioméningite lymphocytaire (LCMV). Nous avons montré qu'une pré-stimulation avec PIL-21 en présence de l'IL-7 ou l'IL-15, les cellules P14 acquièrent la capacité de répondre vigoureusement à des ligands peptidiques modifiés qui montrent une faible activité agoniste envers les cellules P14 naives. Les cellules P14 préstimulées qui sont re-stimulées avec des ligands peptidiques modifiés montrent des puissantes fonctions effectrices telles que la cytotoxicité et la production des cytokines effectrices TNFa et IFNy. Ces cellules induisent le diabète de type 1 lorsqu'elles ont été transférées dans des souris qui expriment l'antigène GP LCMV sous le contrôle du promoteur de l'insuline dans les îlots de Langerhans. Dans l'ensemble, nos résultats montrent que l'IL-15 et l'IL 21 produites durant une réponse inflammation chronique pourraient pré-stimuler des cellules T CD8+ potentiellement autoréactives, conduisant ainsi à des maladies auto-immunes. // Abstract : The activation of naive CD8[superscript +]T cells by an antigen requires two different signals. The first signal is mediated via the T cell receptor (TCR) following its interaction with the peptide presented on class-I major histocompability complex (MHC-I) molecules. The second signal is delivered via the co-stimulatory receptors upon recognition of their ligands on antigen presenting cells. However, in response to homeostatic pressure, as in lymphopenia, naive T cells undergo proliferation without antigenic stimulation through a process referred to as lymphopenia-induced proliferation (LIP). LIP of naive CD8[superscript +] T cells requires IL-7 and a self peptide presented by MHC-I, which implies that TCR signaling is needed for LIP of naive CD8[superscript +]T cells. Recent work from our laboratory has shown that with the homeostatic cytokines IL-7 and IL-15 synergize with IL-21 to induce antigen-independent proliferation of naive CD8[superscript +]T cells. Moreover, this cytokine-driven, antigen-independent proliferation "sensitizes" or "primes" naive CD8[superscript +] T cells to undergo robust proliferation in response to limiting concentrations of their cognate antigens. Cytokine-primed CD8[superscript +]T cells also abundantly produce effector cytokines, such as TNF? and IFN? and display a potent CTL activity following stimulation by antigen when pre-stimulated. In my project, I have investigated whether cytokine-induced priming could be an important mechanism by which potentially autoreactive naive CD8[superscript +]T cells are stimulated to cause autoimmune disease using a TCR transgenic mouse model of autoimmune type 1 diabetes (T1D). These mice harbor CD8[superscript +]T cells that express transgenic P14 TCR (P14 cells), which recognizes an antigenic peptide derived from the glycoprotein antigen (GP33) of lymphocytic choriomeningitis virus (LCMV). We show that, following priming with IL-21 in the presence of IL-7 or IL-15, P14 cells gain the ability to respond robustly to modified peptide ligands that possess weak agonistic activity towards unprimed P14 cells. Furthermore, cytokine-primed P14 cells stmulated with weak TCR ligands displayed potent effector functions such as cytotoxicity and production of effector cytokines, TNF? and IFN?. These cells also induced T1D when adoptively transferred to mice that expressed the LCMV GP antigen under the control of the insulin promoter in the islets. Collectively, our findings show that IL-15 and IL-21 produced during chronic inflammatory conditions could cause priming of potentially autoreactive CD8[superscript +]T cells, leading to autoimmune diseases. [symboles non conformes]

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Anis, Mursalin M. "MODULATION OF NAIVE CD4+ T CELL ACTIVATION AND DENDRITIC CELL FUNCTION IN THE LUNGS DURING PULMONARY MYCOBACTERIAL INFECTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1184427168.

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Reyes-Rodriguez, Angel L. "Dendritic Cells Enhance HIV Infection of Memory CD4+ T Cells in Human Lymphoid Tissues." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1448463150.

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Zhao, Juan, Xindi Dang, Peixin Zhang, Lam Nhat Nguyen, Dechao Cao, Lin Wang, Xiaoyuan Wu, et al. "Insufficiency of DNA Repair Enzyme ATM Promotes Naive CD4 T-cell Loss in Chronic Hepatitis C Virus Infection." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etsu-works/6526.

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T cells have a crucial role in viral clearance and vaccine response; however, the mechanisms regulating their responses to viral infections or vaccinations remain elusive. In this study, we investigated T-cell homeostasis, apoptosis, DNA damage, and repair machineries in a large cohort of subjects with hepatitis C virus (HCV) infection. We found that naive CD4 T cells in chronically HCV-infected individuals (HCV T cells) were significantly reduced compared with age-matched healthy subjects. In addition, HCV T cells were prone to apoptosis and DNA damage, as evidenced by increased 8-oxoguanine expression and γH2AX/53BP1-formed DNA damage foci—hallmarks of DNA damage responses. Mechanistically, the activation of DNA repair enzyme ataxia telangiectasia mutated (ATM) was dampened in HCV T cells. ATM activation was also diminished in healthy T cells exposed to ATM inhibitor or to HCV (core protein) that inhibits the phosphoinositide 3 kinase pathway, mimicking the biological effects in HCV T cells. Importantly, ectopic expression of ATM was sufficient to repair the DNA damage, survival deficit, and cell dysfunctions in HCV T cells. Our results demonstrate that insufficient DNA repair enzyme ATM leads to increased DNA damage and renders HCV T cells prone to apoptotic death, which contribute to the loss of naive T cells in HCV infection. Our study reveals a novel mechanism for T-cell dysregulation and viral persistence, providing a new strategy to improve immunotherapy and vaccine responses against human viral diseases.

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Mochar, Nadine [Verfasser]. "Einflussnahme von proteaseresistenten Peptidliganden auf die T-Zell-vermittelte Immunantwort im Kontext des Typ 1 Diabetes Mellitus / Nadine Mochar." Ulm : Universität Ulm. Medizinische Fakultät, 2016. http://d-nb.info/1081774223/34.

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Alonso, Ramirez Ruby. "Caractérisation in vivo de la réponse des lymphocytes T CD4+ naïfs spécifiques d'un néoantigène à différents stades du développement tumoral." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB099.

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Au cours du développement tumoral, le système immunitaire est constamment exposé aux antigènes tumoraux, mais le plus souvent dans un contexte non-inflammatoire qui favorise l'induction d'une tolérance envers ces antigènes. La tolérance peut être médiée par des mécanismes passifs (ignorance, anergie ou délétion des clones spécifiques de la tumeur) ou actifs, pour lesquels les lymphocytes T régulateurs (Tregs) jouent un rôle prépondérant. Les lymphocytes T (LT) CD4+ sont la source principale des Tregs mais présentent également des fonctions antitumorales directes et indirectes. Les connaissances actuelles sur le rôle des LT CD4+ au cours du développement tumoral proviennent en grande partie d'études de modèles murins de tumeurs transplantées. Cependant, l'inflammation initiée lors de l'inoculation de ces tumeurs due à une mort cellulaire importante favorise la présentation persistante par le MHC-II des antigènes tumoraux dans un environnement inflammatoire artificiel. Nous tentons ici de contourner ce problème en utilisant deux modèles murins différents: le premier est un modèle de tumeur transplantée dans lequel un néoantigène de classe II (DBY) est induit à distance du moment de l'inoculation de la tumeur. Le deuxième est un modèle d'adénocarcinome pulmonaire induit génétiquement exprimant l’epitope DBY, dans lequel la tumorigenèse est initiée par l'expression d’un oncogène associée à la délétion d’un gène suppresseur de tumeurs. La réponse antitumorale des LT CD4+ est suivie par le transfert de LT CD4+ spécifiques de DBY "Marilyn". Dans le modèle de tumeur transplantée, nous montrons que l'apparition d'un néoantigène dans une tumeur bien établie n'est pas ignorée par le système immunitaire. Bien au contraire, le néoantigène arrive au ganglion drainant la tumeur et induit une activation efficace des cellules Marilyn, qui prolifèrent, produisent de l'IFN-γ et recirculent jusqu'à la tumeur. En revanche, malgré une activation efficace des LT CD4+, les tumeurs ne sont pas rejetées. Dans le modèle génétiquement induit, nous montrons que des néoantigènes exprimés dès le début du développement tumoral, arrivent jusqu'au ganglion drainant la tumeur en quantité suffisante pour induire l'activation et la prolifération des LT CD4+, mais que cette activation est non-optimale et ne permet qu'une faible migration vers le site de la tumeur. En revanche, une partie des cellules Marilyn acquièrent l'expression de FOXP3 ainsi qu'une signature transcriptomique de Tregs et ce dès les stades précoces du développement tumoral, tandis que le reste des cellules Marilyn présentent un phénotype anergique (CD44hiCD73hiFR4hi). L'administration de CpG n'empêche pas la conversion en Treg des cellules Marilyn, malgré l'augmentation de la maturation des cellules dendritiques dans le poumon et le ganglion drainant la tumeur. La déplétion des Tregs de l'hôte en revanche inhibe cette conversion et favorise l'activation des cellules Marilyn en cellules effectrices compétentes, capables de migrer jusqu'au site tumoral. Enfin, les cellules Marilyn, lorsqu'elles sont activées hors du ganglion drainant la tumeur échappent à l'inhibition induite par la tumeur et deviennent des cellules effectrices compétentes. Ainsi, dans un modèle tumoral reproduisant le développement naturel progressif des tumeurs humaines, un état de tolérance est induit par la tumeur. Cette tolérance est dépendante des Tregs présents dans le ganglion drainant la tumeur, qui confèrent une tolérance aux LT CD4+ naïfs arrivant dans le ganglion
During tumor development, the immune system is persistently exposed to tumor-associated antigens, frequently in a non-inflammatory context, favoring the establishment of tolerance. Passive (ignorance, anergy or deletion of tumor-specific T cells) or active mechanisms mediated by regulatory T cells (Tregs) may be involved in tolerance. CD4+ T cells are the main source of Tregs but they also display indirect and direct antitumor activity. So far, the contribution of CD4+ T cells during tumor development has been mainly addressed in murine transplanted tumor models. However, in these models the artificial inflammation associated with the presence of dying tumor cells at the time of tumor inoculation favors a long-lasting MHC-II-restricted tumor antigen presentation in an artificial inflammatory context. Here, we addressed this issue using two different models: a transplanted one in which the MHC-II neoantigen (DBY) is induced long after tumor implantation and a genetically engineered mouse (GEM) model of lung adenocarcinoma also expressing the DBY epitope, in which malignant transformation results from both the expression of an oncogene and the deletion of a tumor suppressor gene. Tumor-specific CD4+ T cell response was followed by transfer of naive DBY-specific Marilyn CD4+ T cells. In the transplanted tumor model, we found that the appearance of a neoantigen in established tumors was not ignored by the immune system. On the contrary, the neoantigen reached the tumor-draining lymph node (TdLN) and induced efficient priming of Marilyn cells that proliferated, produced IFN-γ, and recirculated to the tumor site. However, despite efficient induction of a tumor-specific CD4+ T cell response, tumors were not rejected. In the GEM model, we found that starting at the early tumor stages, neoantigens were expressed and reached the TdLN in sufficient amount to induce activation and proliferation of naive Marilyn T cells. However, this priming was suboptimal and resulted in a weak migration to the tumor site. Instead, some of the activated Marilyn cells acquired the expression of FOXP3 and a Treg gene signature while the remaining FOXP3- cells displayed a CD44hiCD73hiFR4hi anergic phenotype. CpG administration did not revert the Marilyn Treg conversion despite reinforcing dendritic cell maturation in the lung and the TdLN. Depletion of the host Treg compartment however, inhibited this conversion and favored Marilyn cell activation into full-blown effector cells able to migrate to the tumor site. Finally, Marilyn cells that were primed at distance of the TdLN, escaped tumor induced inhibition and became full effectors. Thus, in a tumor model reproducing the natural development of slowly growing human tumors, a tumor-associated dominant tolerance is established in the lymph node draining the tumor. This state of unresponsiveness is highly dependent on the presence of Treg cells in the TdLN, conferring tolerance to incoming tumor-specific naive CD4+ T cells

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Okada(Hashimoto), Mutsumi. "The CD70-CD27 interaction during the stimulation with dendritic cells promotes naive CD4[+] T cells to develop into T cells producing a broad array of immunostimulatory cytokines in humans." Kyoto University, 2009. http://hdl.handle.net/2433/126461.

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Chiu, Christopher. "An analysis of the events involved in the differentiation of naive CD8+ T-cells during a primary immune response 'in vivo'." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431697.

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Fukui, Tetsuya. "IL-7 induces proliferation, variable cytokine-producing ability and IL-2 responsiveness in naive CD4[+]T cells from human cord blood." Kyoto University, 1998. http://hdl.handle.net/2433/156990.

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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものである
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第7220号
医博第1971号
新制||医||684(附属図書館)
UT51-98-G149
京都大学大学院医学研究科内科系専攻
(主査)教授淀井淳司, 教授湊長博, 教授古庄巻史
学位規則第4条第1項該当

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Yonkers, Nicole L. "Toll-like Receptor Tolerance in Dendritic Cells During Hepatitis C and HIV Infections: Collapsing the Bridge Between Innate and Adaptive Immunity." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1298412448.

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37

Poch, Tobias [Verfasser]. "Deep immunophenotyping identifies a population of tissue-resident naive-like CD4+ T cells expanded in livers with primary sclerosing cholangitis / Tobias Poch." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/1225041880/34.

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Ogrissek, Nadine [Verfasser], Beatrix [Akademischer Betreuer] Süß, Heinfried H. [Akademischer Betreuer] Radeke, and Ralf [Akademischer Betreuer] Galuske. "Entwicklung einer T-Zelltherapie für chronisch-entzündliche Erkrankungen basierend auf Chemokinrezeptor-Antagonisten / Nadine Ogrissek. Betreuer: Beatrix Süß ; Heinfried H. Radeke ; Ralf Galuske." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2015. http://d-nb.info/1111910049/34.

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Miyamoto, Kazue. "Optimal stimulation for CD70 induction on human monocyte-derived dendritic cells and the importance of CD70 in naive CD4+ T cell differentiation." Kyoto University, 2010. http://hdl.handle.net/2433/120928.

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Nafady-Hego, Hanaa Abdel Hakeem. "The generation of donor-specific CD4+CD25++CD45RA+ naive regulatory T cells in operationally tolerant patients after pediatric living-donor liver transplantation." Kyoto University, 2011. http://hdl.handle.net/2433/142042.

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Fujii, Sumie. "GVHD amelioration by human bone marrow mesenchymal stromal/stem cell-derived extracellular vesicles is associated with peripheral preservation of naive T cell populations." Kyoto University, 2018. http://hdl.handle.net/2433/232136.

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Takao, Sumiko. "The rapid induction of HLA-E is essential for the survival of antigen-activated naive CD4 T cells from attack by NK cells." Kyoto University, 2011. http://hdl.handle.net/2433/142088.

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Auma, Ann Winniefred Nangobi. "THE IMPACT OF DIRECT-ACTING ANTI-VIRAL THERAPY ON NAIVE CD4+ T CELL LYMPHOPENIA AND CELLULAR IMMUNE ACTIVATION IN HCV INFECTION AND HCV/HIV CO-INFECTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1625764728651756.

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44

Tonon, Sandrine. "La toxine de Bordetella pertussis active les cellules dendritiques et les lymphocytes T CD4 naïfs chez l'homme." Doctoral thesis, Universite Libre de Bruxelles, 2006. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210749.

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La toxine de pertussis (PTX) est une A-B protéine considérée comme l’un des principaux facteurs de virulence de Bordetella pertussis, l’agent bactérien responsable de la coqueluche. Aujourd’hui, cette maladie représente encore un réel danger pour les nouveaux-nés et les

nourrissons non ou partiellement immunisés. Actuellement, la coqueluche provoque encore la

mort d’environ 350.000 individus par an. La toxicité de la PTX est liée à l’activité

enzymatique de sa sous-unité A capable d’inhiber les voies de signalisation associées aux

protéines Gi. La partie B, quant à elle, permet l’entrée de cette sous-unité A dans le

cytoplasme des cellules cibles en se liant spécifiquement à son ou ses récepteurs

membranaires toujours inconnus de nos jours.

Des études réalisées chez la souris et chez l’homme ont montré que les vaccins anticoquelucheux combinés à différents antigènes vaccinaux étaient capables de moduler

leurs réponses humorales spécifiques. Par ailleurs, la PTX est couramment qualifiée d’agent

immunostimulant. En effet, des modèles murins de vaccination permirent d’identifier des

propriétés adjuvantes de la PTX coadministrée avec des antigènes non relevants.

Le travail développé dans ce manuscrit étudie les effets de la PTX sur 2 types cellulaires

primordiaux sollicités lors d’une vaccination :la cellule dendritique (DC) et le lymphocyte T

CD4+ naïf.

Les DC sont les seules cellules présentatrices d’antigènes aptes à initier une réponse immune

primaire. Dans un premier temps, nous avons montré que la PTX était capable d’activer des

DC générées in vitro à partir de monocytes. En effet, elles acquièrent un phénotype mature

caractérisé par une augmentation de l’expression membranaire des molécules costimulatrices

et du CMH de classe II, démontrant un effet direct et spécifique de la PTX sur les DC

myéloïdes. Parallèlement, ces DC produisent du TNF-a, de l’IL-12p40 et de l’IL-12p70 et

activent NF-kappaB, un facteur de transcription essentiel au processus de maturation. Nous

avons obtenu des résultats similaires avec une toxine génétiquement modifiée qui est

enzymatiquement inactive. A partir de sang total incubé avec la PTX, nous avons par ailleurs

observé que les DC circulantes du nouveau-né étaient déficientes dans leur maturation et leur

sécrétion d’IL-12p70 comparées aux DC de l’adulte.

D’autre part, il a été décrit précédemment que la PTX exerçait des effets mitogènes sur les

lymphocytes T humains et murins. Cependant, le rôle qu’elle joue sur la population des

lymphocytes T CD4 naïfs reste peu connu. A l’issue de notre second travail, nous pouvons

dès lors affirmer que la PTX est également capable d’activer des lymphocytes T

CD4+CD45RA+ naïfs isolés à partir des cellules mononuclées du sang périphérique, et ce

indépendamment de son activité enzymatique. En effet, ces lymphocytes T CD4+ naïfs stimulés par la PTX prolifèrent, synthétisent des quantités non négligeables d'ARN messagers

codant pour l’IL-2 et le TNF-a, augmentent l’expression membranaire des molécules CD40L,

CD69 et CD25 et expriment la protéine Foxp3. Cette activation s’accompagne de la translocation nucléaire de NF-kappaB et NFAT. Parallèlement à l’adulte, la PTX active les lymphocytes T CD4 néonataux. Néanmoins, ceux-ci prolifèrent moins bien et expriment plus faiblement le CD40L à leur surface.

Enfin, la PTX induit la sécrétion de taux importants d’IFN-g par des T CD4+CD45RA+ naïfs

adultes mis en présence de DC autologues.

Nous terminerons en proposant l’hypothèse suivante :La PTX pourrait exercer ses propriétés

adjuvantes par l’intermédiaire de différents mécanismes comprenant notamment la maturation

des DC d’origine myéloïde et l’activation des lymphocytes T CD4+CD45RA+ naïfs. Ces 2 populations cellulaires sont en effet les principaux protagonistes impliqués dans la réponse

immune primaire.
Doctorat en sciences pharmaceutiques
info:eu-repo/semantics/nonPublished

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Skrzipek, Sabine Susanne Nadine [Verfasser]. "In vitro Effekte von Interferon-β1b auf Zytokinsekretion und Proliferation von T-Lymphozyten-Subpopulation von Gesunden und Patienten mit schubförmiger Multipler Sklerose und Patienten mit primär progredienter Multipler Sklerose / Sabine Susanne Nadine Skrzipek." Greifswald : Universitätsbibliothek Greifswald, 2012. http://d-nb.info/1027606180/34.

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Albert, Loïc. "Le recherche de naines brunes d'étoiles du voisinage solaire et le spectrographe multi-objets SIMON." Thèse, 2006. http://hdl.handle.net/1866/17369.

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Judokusumo, Edward. "Mechanosensing in Naive CD4+ T cells." Thesis, 2014. https://doi.org/10.7916/D81G0JFM.

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T cells are key players in adaptive immune response. Originating from the thymus, they seek and eliminate infected cells in various locations of our body. T cells are not anchorage-dependent in nature. However, in our body, cells are constantly under physiological stress. It is not yet known how natural changes in physical environment could affect T cell behaviors. This thesis focuses to study the role, pathway, and main mechanism of rigidity sensing in T cells. Most studies of T cell rigidity sensing have showed that T cell responses are sensitive to external forces. It is unclear whether T cells could generate forces, translate them to biochemical signaling, and regulate their function based on the physical sensing. We tested the idea by developing the use of substrate with varying modulus to analyze the impact of rigidity to T cell activation. We demonstrated that mouse naive CD4+ T cells were capable of sensing and transmitting information from substrate modulus, ultimately affecting the regulation of cytokine secretion, a key indicator of T cell activation. Interestingly, this cytokine secretion correlated with increasing substrate rigidity. This increased cytokine secretion diminished when T cells lost the ability to contract in sensing the underlying substrate rigidity. Contrary to the presumption that T cells are not able to regulate their function based on the forces applied to the environment, our study provides the first demonstration that substrate rigidity has a functional impact to naive CD4+ T cell activation. To understand the translation process from physical to biochemical signaling in T cells, we determined the signaling pathway that regulated T cell rigidity sensing. We found that T cell rigidity sensing was associated with the signaling molecules of the T cell receptor (TCR) complex, the central pathway of T cell response. Analysis of TCR signaling molecules revealed that T cell rigidity sensing was mediated downstream of the early signaling components in the TCR complex. Lastly, we developed a method of combining micron-scale patterning in elastic substrates to determine whether T cell mechanosensing was mediated from local adhestion sites or globally throughout the cell. Circular features of primary signal for naive CD4+ T cells were spatially segregated and patterned on elastic substrates to analyze T cell contractility in generating forces across the segregated primary signals, leading to sustained TCR triggering. We found out that T cell contractility failed to generate forces when the primary signals were arranged in equilateral triangle geometry, leading to loss of TCR triggering. This result shows that T cell rigidity sensing is mediated globally throughout the whole cell rather than locally from adhesion sites. Furthermore, the loss of TCR triggering by T cells when sensing the equilateral triangle geometry in elastic substrates opens up new ideas in characterizing force generation within the cell.

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Artigau, Étienne. "Variabilité temporelle des naines T et construction d'une caméra infrarouge à grand champ." Thèse, 2005. http://hdl.handle.net/1866/17376.

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"Contact-dependent activation of macrophages by naive CD4+ T cells." East Tennessee State University, 2000. http://etd-submit.etsu.edu/etd/theses/available/etd-0602100-130806/.

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Shy-Ni, Wen, and 文詩妮. "Functional Fate of Naive CD8+ T cells activated by PMA + Ionomycin + IL-4." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/68146693751383761228.

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Abstract:

碩士
國立臺灣大學
免疫學研究所
87
According to distinct cytokine secreting profile, CD8+ T cells can be defined as two populations : type 1 or Tc1 T cells that secret IL-2, IFN- and TNF- ; type 2 or Tc2 T cells that secret IL-4, IL-5 and IL-10. The presence of IL-4 in primary activation culture will drive CD8+ T cells to differentiate into Tc2 phenotype. In vivo persistence of type 1 and type 2 polarization have been documented in CD4+ and CD8+ T cells. The reports demonstrated that both in CD4+ and CD8+ T cells, neither type 1 or type 2 T cells would change their cytokine secreting profile after surviving in vivo. PMA and ionomycin are mitogens for T cells. The combine actions of PMA + ionomycin + IL-4 can induce naive CD8+ T cells to down-regulate surface CD8 expression, undergo Tc2 differentiation and express efficient cytotoxic activity. The main purpose of this study is to identify the functional fate of naive CD8+ T cells activated in vitro by PMA + ionomycin + IL-4. Specifically, stability and potential reversibility with respect to IL-4 producing ability, loss of CD8 expression and ctyotoxic activity were examined. The results indicated that conferred IL-4 producing ability of B10 T cells can persist in vivo but 2C tg T cells can not retain this functional characteristic. Down-regulation of CD8 expression is irreversible both in B10 and 2C tg T cells. Activated B10 T cells are potent cytotoxic effectors, and their potentials of regaining cytotoxic activity can exist in vivo.

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