Dissertations / Theses on the topic 'FOXP4'
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Campbell, Andrew J. "The role of FOXP4 and FOXP2 in haematological malignancy." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510935.
Full textMendoza, Ezequiel [Verfasser]. "FoxP1, FoxP2 and FoxP4 in the song control system of zebra finches: molecular interactions and relevance for vocal learning / Ezequiel Mendoza." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1026695775/34.
Full textKozma, Radoslav. "Inferring demographic history and speciation of grouse using whole genome sequences." Doctoral thesis, Uppsala universitet, Zooekologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-299926.
Full textGoatly, Alison. "FOXP1 abnormalities in lymphoma." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611626.
Full textBaumann, Katrin [Verfasser]. "DNA-Methylierungsmuster im foxp3 Gen in humanen CD4+ FOXP3-exprimierenden T-Zellen / Katrin Baumann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023494183/34.
Full textNishioka, Tomohisa. "CD4[+]CD25[+]Foxp3[+] T cells and CD4[+]CD25[-]Foxp3[+] T cells in aged mice." Kyoto University, 2007. http://hdl.handle.net/2433/135647.
Full textTse, Yuen-yu Belinda, and 謝宛余. "Expression of FOXP1 in breast cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193527.
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Tolosa, Montero Mª Amparo. "Gen FOXP2: Esquizofrenia, alucinaciones auditivas y lenguaje." Doctoral thesis, Universitat de València, 2009. http://hdl.handle.net/10803/9945.
Full textThis thesis has focused in the study of FOXP2 gene, which is the first gene related to a language disorder and which has been subject to positive selection in human lineage, as candidate gene for schizophrenia through different approaches Case-control study didn't allow establishing a consistent relationship between the analyzed structural variants (SNPs and trinucleotide repetitions) and auditory hallucination as alternative phenotype for schizophrenia. Nevertheless, a role of FOXP2 in vulnerability to schizophrenia through its relationship with language cannot be ruled out since SNP rs2396753 showed a trend to significance and SNP rs2253478 showed significative differences for Poverty of Speech. Analysis of promoter region suggests regulation of the expression of the gene is more complex than it was initially expected.Evolutionary analysis of a 6Kb fragment surrounding first exon of the gene revealed different evolutionary rates in different fragments as well as some potential promoter regions. A highly conserved region was detected upstream of the annotated promoter. In order to determine if this highly conserved region should be included in the promoter core functional analyses were performed. These experiments indicated that this region probably contains repressor elements. Under the epigenetic hypothesis of the origin of schizophrenia an analysis of the methylation patterns of a CpG island adjacent to first untranslated was performed. Differences between upstream and downstream region were detected as well as differences for methylation of parahippocampal gyrus in patients and controls and between hemispheres. Quantification of mRNA levels was conducted in order to correlate methylation and expression levels of the gene, with inconclusive results.As a summary, with our results we cannot rule out a role of FOXP2 in the susceptibility to schizophrenia, although no direct evidence has been obtained.
Lindmayer, Christian [Verfasser], and Sebastian [Akademischer Betreuer] Grundmann. "Die Rolle des Transkriptionsfaktors FoxP1 beim Blutgefäßwachstum." Freiburg : Universität, 2021. http://d-nb.info/1236846036/34.
Full textRamcke, Torben [Verfasser]. "The function of RORγt+Foxp3+ biTregs in glomerulonephritis : Die Rolle von RORγt+Foxp3+ biTregs im Rahmen der Glomerulonephritis / Torben Ramcke." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2019. http://d-nb.info/1221721011/34.
Full textStoppe, Muriel. "Synaptische Plastizität im Kleinhirnkortex von FoxP2-mutanten Mäusen." Doctoral thesis, Universitätsbibliothek Leipzig, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-81212.
Full textSather, Blythe Duke. "CD4+ Foxp3+ regulatory T cell homing & homeostasis /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8343.
Full textPeter, Christian. "mTOR signalling and the regulation of FOXP3 expression." Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.600239.
Full textMedvedeva, Vera. "Characterization of Foxp2 functions in the mouse cortex." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066118/document.
Full textGenetic disruptions of the forkhead box transcription factor FOXP2 in humans cause a severe autosomal-dominant speech and language disorder. FOXP2 expression pattern and genomic structure are highly conserved in distant vertebrates. We hypothesized that this conservation may allow the use of animal models to identify Foxp2 dependent neuronal circuits and molecular networks involved in social behaviors. Therefore I began characterizing Foxp2 functions in the mouse cortex in conventional heterozygous (Foxp2+/-) and conditional (cortex specific) Foxp2 homozygous mutant mice (Nex-Cre; Foxp2lox/lox). Initial characterization of Nex-Cre; Foxp2lox/lox mice revealed no gross alterations in morphological architecture, postnatal development and basic adult behaviors. However, behavioral profiling of Nex-Cre; Foxp2lox/lox mice demonstrated deficiency in specific social behaviors such as approach behavior towards conspecifics and responses of WT interaction partners. Furthermore, Nex-Cre; Foxp2lox/lox mice showed alterations in specific acoustical parameters of ultrasonic vocalizations (USV), and the type of modulation differed in function of social context. Gene expression profiling of Foxp2-positive cortical pyramidal neurons in Foxp2+/- mice revealed the dysregulation of Mint2, a gene involved in approach behavior in mice and autism spectrum disorder in humans. This result was further validated in cortex-specific Foxp2 mutant mice The results deliver first insights into cortical Foxp2 dependent functions in mouse social behaviors. This provides a rational basis for further mechanistic studies of the ancestral functions of cortical Foxp2 that may have been recruited during speech and language evolution
Lehnert, Jonathan [Verfasser], and Niklas [Gutachter] Bayersdorf. "Einfluss von Osteopontin auf Foxp3-negative konventionelle und Foxp3-positive regulatorische CD4-positive T-Zellen der Maus / Jonathan Lehnert ; Gutachter: Niklas Bayersdorf." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1204366802/34.
Full textOcklenburg, Frank. "Bedeutung des Transkriptionsfaktors Foxp3 für die T-Zell-Funktion." [S.l. : s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976625423.
Full textNissen, Jesper Klintø. "Control of regulatory T cell lineage differentiation by Foxp3." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609792.
Full textZuber, Julien. "Physiologie et pathologie des cellules régulatrices CD4+CD25+FOXP3+." Paris 6, 2007. http://www.theses.fr/2007PA066178.
Full textDouglass, Stephen Mark. "The roles of FOXP3 and CXCR4 in breast cancer." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2402.
Full textGivel, Anne-Marie. "Rôles de CXCL12beta dans l'hétérogénéité fibroblastique et l'immunosuppression dans les cancers de l'ovaire." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC222.
Full textEpithelial ovarian cancers are the first cause of death from gynecologic cancer. We focusedour work on high-grade serous ovarian cancer (HGSOC) patients, for who only very fewtherapeutic options exist. In the past, several laboratories, including ours, have identified -based on transcriptomic data- distinct molecular subgroups amongst HGSOC. Interestingly,among these different molecular subgroups, one of them, referred to as “Fibrosis” or“Mesenchymal” is systematically identified and consistently associated with poor patientprognosis in all studies. Transcriptomic signature that defines this specific molecularsubgroup of HGSOC contains mainly genes involved in extracellular matrix remodeling andstromal composition, suggesting a potential role of stroma and Carcinoma-AssociatedFibroblasts (CAF) in this particular “Fibrosis/Mesenchymal” HGSOC subgroup.By combining various technics studying concomitantly 6 different CAF markers, we identifiedfor the first time 4 different subpopulations of CAF in HGSOC. Interestingly, one of thesesub-populations, referred to as CAF-S1, significantly accumulates in the“Mesenchymal/Fibrosis” subgroup of HGSOC. Importantly, we demonstrated that the CAFS1cellular subpopulation exhibits immunosuppressive activities. Indeed, CAF-S1 fibroblastsnot only by attract regulatory T lymphocytes but also promote their survival and activation(assessed by expression of FOXP3). Finally, we uncovered the specific role of the CXCL12βisoform as an important player of CAF-S1 identity and immunosuppressive functions inmesenchymal HGSOC.All together, these results identify a stromal heterogeneity in HGSOC, which has beenbroadly underestimated until now. Moreover, our work demonstrates the accumulation of aCAF subpopulation with immunosuppressive functions in HGSOC mesenchymal patients thatcould account, at least in part, for their poor survival rate. Deep characterization of thestroma may enable us to define new therapeutic options combining CAF-targeting therapiesand immunotherapies, in order to improve survival of HGSOC mesenchymal patients
Redpath, Stephen Alexander. "Role of ICOS in Foxp3+ Treg responses induced by parasitic helminths." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/7649.
Full textCavalcanti, Yone Vila Nova. "Avaliação do perfil de produção e expressão de mediadores da resposta imune celular em comunicantes e indivíduos com história de tuberculose pulmonar." Universidade Federal de Pernambuco, 2012. https://repositorio.ufpe.br/handle/123456789/10986.
Full textMade available in DSpace on 2015-03-06T11:29:09Z (GMT). No. of bitstreams: 2 tese Yone-final-20-12-12.pdf: 714270 bytes, checksum: 2a36b003dfa84355204e28d809e01cff (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Previous issue date: 2012
A tuberculose pulmonar é um problema de saúde pública mundial e apresenta alta incidência no Brasil. Atualmente, o Brasil ocupa o 19º lugar no ranking dos 22 países que concentram 80% dos casos em todo o mundo. A resposta imune humana contra a tuberculose é especialmente mediada pelos linfócitos T CD4+. Entretanto, muitos estudos ainda são necessários para o entendimento exato do papel de cada citocina no mecanismo de cura da doença. A fim de caracterizar a produção das citocinas TNF-a, IFN-g, IL-10, o óxido nítrico (NO) e a expressão do marcador Foxp3, células mononucleares do sangue periférico (PBMC) de contatos intradomiciliares de indivíduo com tuberculose pulmonar com (CTb) e sem (STb) história prévia de TB foram estimuladas in vitro com antígeno de Mycobacterium tuberculosis (AgTb) e com o mitógeno Concanavalina A por 24 e 48 horas. A dosagem das citocinas foi feita por ELISA de captura e de NO pela quantificação do nitrito (NO2 -). PCR em Tempo Real foi a técnica utilizada para detectar o mRNA para Foxp3. Em 24 horas de cultivo celular com antígeno total de M. tuberculosis (CTb = 10.158,38 ± 7.438,38; STb = 15.083,10 ± 9.292,66), observou-se uma produção significativa de TNF-a (0,05) no grupo STb. Os grupos analisados não apresentaram diferenças na expressão do mRNA do marcador Foxp3. Foi verificado aumento (p= 0,04) entre IL-10 e Foxp3 e correlação negativa (p = 0,009) entre NO (aumento) e Foxp3 (diminuição) após 48h de estímulo com AgTb. Observou-se também no grupo STb em 24 horas de culturas estimuladas com AgTb um resultado semelhante ao grupo CTb (p = 0,03). Portanto, os resultados obtidos sugerem que produção de IL-10, IFN-g e de NO indicam que os indivíduos CTb e STb produziram uma resposta celular específica; porém, sem valores que possam indicar uma maior ou menor susceptibilidade à doença, e que TNF-a, possivelmente funciona como um elemento fundamental para a manutenção do estado de saúde dos comunicantes. A expressão do marcador Foxp3 não está associada diretamente a uma maior predisposição nos indivíduos com história de tuberculose pulmonar.
Hermans, Cecilia. "CCL22, CD8 und FoxP3 als prognostische Marker beim fortgeschrittenen Ovarialkarzinom-." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-163564.
Full textLin, Li. "The role of FoxN4 in regulating interneuron specification during development." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32562.
Full textCette étude a pour but d'étudier le développement neuronal du réseau locomoteur spinal chez les vertébrés responsable de la génération intrinsèque des activités motrices rythmiques. Les interneurones (INs) de la classe V2 de la moelle épinière ventrale des embryons de poussins et de souris sont divisés en groupes V2a et V2b. Les sous-classes V2 ont des phénotypes de neurotransmetteurs opposés, avec les V2a étant identifiés comme étant glutamatergiques et excitateurs tandis que les V2b sont GABAergiques et inhibiteurs. Leur spécification durant le développement a été attribué à l'expression du facteur de transcription Foxn4. Par contre des expériences récentes de sur-expression chez le poussin ont données des résultats contradictoires à savoir si le Foxn4 est suffisant pour induire les INs V2b et aussi pour supprimer la destinée V2a. Je me suis servie du modèle beaucoup plus simple de l'embryon du poisson zébré avec moins de neurones afin de valider le rôle de la foxn4. Dans un premier temps j'ai caractérisé l'expression de différents transcrits à des stages différents du développement chez le poisson zébré. J'ai ainsi confirmé l'expression d'un transcrit embryonnaire spécifique et j'ai trouvé que tous les transcrits sont supprimés chez le poisson adulte. J'ai aussi déterminé l'identité cellulaire des INs V2b chez le poisson zébré par double marquage par hybridisation in situ et par immunocytochimie, ce qui a confirmé que ces INs ventraux sont GABAergiques. Afin d'altérer les populations V2a et V2b j'ai soit surexprimé l'ARNm du foxn4 ou réduit son expression par injection d'un oligonucléotide morpholino antisens a
Chang, Xing. "X-Linked FOXP3 & OTC in immune tolerance and autoimmunity." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1149171466.
Full textZuo, Tao. "FOXP3 is a novel X-linked breast cancer suppressor gene." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1150079443.
Full textKendal, Adrian R. "The role of FOXP3+ regulatory T-cells in transplant tolerance." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558327.
Full textEvans, Amy E. "Characterisation of Foxp1 in striatal development and the adult brain." Thesis, Cardiff University, 2013. http://orca.cf.ac.uk/58414/.
Full textLalfer, Mélanie. "Propriétés de reconnaissance antigénique des lymphocytes T régulateurs CD4+ FOXP3+." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB109.
Full textNo abstract available
Taguchi, Nanae. "HTLV-1 bZIP Factor Induces Inflammation through Labile Foxp3 Expression." Kyoto University, 2013. http://hdl.handle.net/2433/180612.
Full textAllan, Sarah E. "Defining the biological role of FOXP3 in human CD4+ T cells." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1122.
Full textButz, Martin Benedikt. "Erhöhte Anzahl von CD25⁺FOXP3⁺ regulatorischen T-Zellen im oralen Plattenepithelkarzinom /." Regensburg, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254407.
Full textFontenot, Jason David. "The role of Foxp3 in CD4⁺ T cell development and function /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/8336.
Full textHolmes, Derek Allan Su Lishan. "Modulation of HIV-1 replication and T cell activation by FoxP3." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1598.
Full textTitle from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.
Freyer, Jennifer Sandra Silvia. "Regulation und funktionelle Rolle des murinen Transkriptionsfaktors Foxp3 in T-Zellen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15841.
Full textThe aim of the study was to analyze the function and regulation of the transcription factor Foxp3. In a first step we designed a BAC-transgenic mouse with eYFP under the control of the Foxp3 promoter. For creating these mice we use the ET- cloning method. The step of homologous recombination of the target vector into the BAC failed. Because of that, we decided to work in cooperation with the group of Tim Sparwasser from Munich and their BAC- transgenic mouse called DEREG- mouse. This mouse expresses the coding region of eGFP fused to the diphtheria- toxin- receptor under the control of the Foxp3 promoter. Therefore Foxp3+ T cells can be easily detected by eGFP expression and can even be depleted by diphtheria- toxin- application. We confirmed the co- expression of Foxp3 and eGFP and furthermore tested the functionality of the depletion- process of Foxp3+ T cells by treatment with diphtheria- toxin. In a second study, we analyzed the stability of Foxp3 expressing cells in vivo. Therefore we transferred Foxp3+ T cells in syngenic mice and analyzed these cells after 14 days for their Foxp3- expression. Furthermore, we tested the induction of Foxp3 expression through TGF-beta and the suppressive activity of these cells. We also analyzed those cells for their methylation pattern, comparing cells, which showed an induction of Foxp3- expression after one week of culture with TGF-beta to cells, which received TGF-beta for one week and were then restimulated in the absence of TGF-beta. The stability of Foxp3 expression seems to correlate with the demethylated state of the TSDR (Treg Specific Demethylated Region). To get a closer look on the region called TSDR in the murine foxp3 locus, we decided to analyze this region under different aspects. First, we checked for putative binding sites of transcription factors by database analysis of the TSDR. We also analysed histon modifications, such as acetylation of histon H3 and H4 and tri- methylation of lysine 4 at histon3, in this region. Presence of these modifications hinted an epigenetic regulation of Foxp3 involving the TSDR. In a last step, the transcriptional activity of TSDR was tested to delineate whether the TSDR serves as an alternative promoter or acts as a regulative element like an enhancer. Luciferase assays showed that TSDR is a regulative enhancer element, which loses transcriptional activity when methylated. Deletion mutants determined the most important fragment of the TSDR.
Kaur, Gurman. "Functional characterisation of Foxp3 splice variants in human regulatory T cells." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611427.
Full textRibot, Julie. "Etude du développement thymique des lymphocytes t régulateurs CD4+ CD25+ Foxp3+." Toulouse 3, 2006. http://www.theses.fr/2006TOU30221.
Full textHändel, Norman. "Die Rolle von Interleukin-2 für die Interaktion von Foxp3+ regulatorischen T-Zellen mit Effektorzellen im Darm." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-67596.
Full textBauch, Michael. "Immunregulation durch mukosale regulatorische Foxp3 positive T-Zellen bei Kindern und Jugendlichen mit Zöliakie." Doctoral thesis, Universitätsbibliothek Leipzig, 2012. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-96784.
Full textLago, Fernanda. "Perfil imunoistoquímico de linfócitos T regulatórios no pênfico foliáceo endêmico através da expressão do marcador Foxp3." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5133/tde-01122011-194907/.
Full textBackground: CD4+CD25+Foxp3+ regulatory T cells (Tregs) play a crucial role in the maintenance of self tolerance and control of the magnitude of the immune response. Their quantitative or functional impairment has been reported in several autoimmune disorders. Endemic pemphigus foliaceus (EPF) is an autoimmune organ-specific blistering skin disorder that shares many clinical and immunopathological features with classic pemphigus foliaceus, but with unique epidemiological features. Circulating and tissue-bound IgG auto-antibodies react against desmosomal cadherins (desmoglein 1), causing loss of adhesion between keratinocytes. Aims: The purpose of this study was to evaluate whether the loss of tolerance is associated with impairment of CD4+CD25+Foxp3+ Tregs in the skin of EPF patients. Methods: Skin samples from 22 patients and 10 controls were submitted to immunohistochemistry with anti-CD4, CD25 and Foxp3. Photomicrographs were obtained from consecutive fields along epidermis and dermis; quantification of Foxp3+, CD4+, CD25+, CD4+Foxp3+ and CD25+Foxp3+ cells were performed in each compartment, taking into account the respective field area (m2). Significance was set at p<0.05. Results: We found an enhanced epidermal infiltrate of CD25+(p=0.003), Foxp3+(p=0.04) and CD25+Foxp3+(p=0.007) immunostained T cells in EPF patients, when compared to controls. Dermal infiltrate exhibited a higher expression of CD4+ (p<0.001) and CD25 p=0.008) T cells in EPF skin samples than in controls. Conclusions: Our findings suggest that the break of peripheral immunologic tolerance in EPF patients did not correlate with an impairment of CD4+CD25+Foxp3+ Treg cells present in the affected skin. However, higher expression of CD25+Foxp3+ cells in the epidermal infiltrate could be a counterpart of a diverse population of T cells, previously described as exerting a regulatory activity, yet to be defined
Vernes, Sonja. "Investigation of the role of FOXP transcription factors in neurodevelopment." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497468.
Full textYao, Edmund. "Effects of DNA methyltrasferase-inhibition on FOXP3 expresssion in CD4+ T cells." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110525.
Full textABRÉGÉLes lymphocytes T régulateurs CD4+Foxp3+ (TREG) sont des pivots dans le maintien de la tolérance immunitaire aux antigènes autologues et agissent en tant que régulateurs des réactions auto-immunes. Il y a deux sous-ensembles de TREG : les naturelles (nTREG) qui se développent dans le thymus et les inductibles (iTREG) qui sont générés à partir des lymphocytes T effecteurs Foxp3- conventionnels (TCONV) en périphérie ou in vitro. Bien que les deux sous-ensembles requièrent l'expression de Foxp3 pour fonctionner, les lymphocytes iTREG régulent graduellement de manière négative Foxp3 in vitro et perdent leur capacité suppressive. En revanche, les lymphocytes nTREG présentent une expression constitutive de Foxp3 et démontrent une fonction suppressive stable in vitro. Des études récentes révèlent une région du locus Foxp3 qui est différentiellement méthylée entre les nTREG et les iTREG. La région sensible à la méthylation, connue sous le nom de la région déméthylée spécifique à TREG (TREG-specific demethylated region, TSDR), est complètement non méthylée dans les nTREG, partiellement méthylée dans les iTREG, et fortement méthylée dans les TCONV. Cela suggère que les modèles de méthylation différentielle du TSDR pourraient expliquer l'expression instable de Foxp3 dans les iTREG. Les enzymes ADN méthyltransférases (DNA methyltransferases, DNMTs) servent de médiatrices dans la méthylation, et quelques inhibiteurs sont connus pour bloquer leur activité. Dans cette étude, nous utilisons le 5'-Aza-2'-déoxycytidine (Aza), un inhibiteur analogue nucléosidique, et RG108, un inhibiteur non-nucléosidique, pour déterminer si l'inhibition des DNMTs et ainsi la méthylation, aurait un impact sur l'expression de Foxp3 et le développement de iTREG en culture. Nos résultats montrent que l'inhibition de DNMT en l'absence de TGF-β n'a pas pu induire l'expression de Foxp3 dans les lymphocytes TCONV. Toutefois, dans les lymphocytes TCONV qui étaient pré-exposés au TGF-β, Aza et RG108 ont induit l'expression de Foxp3 dans un nombre important de lymphocytes. De plus, une proportion plus grande de lymphocytes exprimant le Foxp3 avec un Foxp3 MFI plus élevé étaient induits lorsque Aza était utilisé conjointement avec TGF-β, suggérant un effet additif et non redondant de l'inhibition de DNMT. Malgré que les lymphocytes iTREG régulent généralement de façon négative Foxp3 en l'absence de TGF-β, le traitement par Aza seul prolonge la persistance de l'expression de Foxp3. Ni Aza, ni RG108 n'est aussi efficace que TGF-β dans le maintien de l'expression de Foxp3. En somme, nos données montrent que l'inhibition de DNMT sans TGF-β est insuffisant pour induire l'expression de Foxp3, mais que conjointement, peut en augmenter l'induction et la renforcer. L'inhibition de DNMT peut également prolonger l'expression de Foxp3 en l'absence de TGF-β possiblement en perturbant les mécanismes d'inhibition épigénétique.
Elahi, Mojdeh Fanny. "Functional studies of FOXP2-gene involved in brain development and language acquisition." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531813.
Full textMarticke, Simone Sigrid. "Ultra-high throughput sequencing analysis of FOXP2 occupancy in the human genome /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Full textCuss, Steven Martin. "The CD40-CD154 pathway in the development of Foxp3⁺ regulatory T cells." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610532.
Full textMarguti, Ivo. "Efeito das células dendríticas na geração de células T CD4+CD25+Foxp3+." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-18102007-154828/.
Full textDendritic cells (DCs) are the most important antigen-presenting cells of the immune system. However, DCs have also been implicated in maintaining immunologic tolerance. CD4+CD25+Foxp3+ T lymphocytes are known as cells with regulatory properties. In this study we evaluated the changes in the CD4+CD25+Foxp3+ T cell population after co-culture of lymph-node cells with DCs. Our results show an increase in the CD4+CD25+Foxp3+ T cell population after co-culture and occurs regardless of the activation state of DCs and the presence of exogenous antigens; however it is greater when immature DCs are previously pulsed with exogenous antigen. We also noticed that TGF-? is present in all cultures conditions in which the CD4+CD25+Foxp3+ T cell population increases. Our data also suggests that the increase of the CD4+CD25+Foxp3+ T cell population may be due to the proliferation of these cells.
Cassan, Cécile. "Lymphocytes T CD4+Foxp3+ régulateurs et auto-immunité du système nerveux central." Toulouse 3, 2006. http://www.theses.fr/2006TOU30184.
Full textThe immune system defends us against invasions of pathogens; meanwhile, several mechanisms, including the control exerted by CD4+CD25+Foxp3+ regulatory T lymphocytes (Tregs), maintain an immune tolerance towards self-antigens. A disruption of this tolerance contributes to the development of auto-immune diseases, such as multiple sclerosis (MS). We have showed that Tregs protect mice against the development of experimental auto-immune encephalomyelitis (EAE), which is an animal model for MS. We have then investigated the role of the thymus and of self-antigens in the generation of Tregs specific for central nervous system antigens, as well as their specificity in EAE. A better knowledge on Tregs will allow the design of new therapeutic strategies for MS patients
Kotey, Amos. "Newly Identified Role for the Transcription Factor Foxp1 in Natural Killer Cells." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1627658577374061.
Full textAkbar, Haroon. "Rôle des cellules T régulatrices dans un modèle murin de toxoplasmose aigüe." Thesis, Tours, 2011. http://www.theses.fr/2011TOUR3803/document.
Full textLong term concomitant immunity is developed in case of persistant infections with intracellular protozoan parasites like for example in leishmaniosis and malaria. In a murine model of leishmaniosis, it has been demonstrated that CD4+CD25+ regulatory T (Treg) cells are involved in the persistance of leishmania parasites at cutaneous sites of infection and protect the host against re-infection.The protozoan parasite Toxoplasma gondii is also responsible for a chronic infection associated with the settlement of parasite in the brain and the muscles of the host in the form of cysts. It was therefore pertinent to know about the implication of Treg cells in the development and the persistance of toxoplasma. To attain this objective, we have used a monoclonal antibody anti-CD25 in depletion experiments during the acute phase of toxoplasmosis after infection of outbred mice with a type II toxoplasma strain. No significant difference was found in terms of mortality or in brain cyst load between depleted mice and non-depleted mice. In addition to these experiments, we have shown that not only the CD4+CD25+Foxp3+ regulatory T (Treg) cells but also the CD4+CD25+Foxp3- T effector (Teff) cells are a potential target of anti-CD25 antibody-depletion. These cells are induced to express CD25 during acute phase of the infection
Döbbeler, Marina [Verfasser], Alexander [Akademischer Betreuer] Steinkasserer, and Falk [Gutachter] Nimmerjahn. "Die endogene CD83 Expression auf Foxp3+ T-Zellen ist essenziell für die Differenzierung und Funktion muriner Foxp3+ regulatorischer Effektor-T-Zellen / Marina Döbbeler ; Gutachter: Falk Nimmerjahn ; Betreuer: Alexander Steinkasserer." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2018. http://d-nb.info/1169399061/34.
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