Please use this identifier to cite or link to this item: http://buratest.brunel.ac.uk/handle/2438/5677
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dc.contributor.authorAnderson, PO-
dc.contributor.authorManzo, BA-
dc.contributor.authorSundstedt, A-
dc.contributor.authorMinaee, S-
dc.contributor.authorSymonds, A-
dc.contributor.authorKhalid, S-
dc.contributor.authorRodriguez-Cabezas, ME-
dc.contributor.authorNicolson, K-
dc.contributor.authorLi, S-
dc.contributor.authorWraith, DC-
dc.contributor.authorWang, P-
dc.date.accessioned2011-07-29T08:57:10Z-
dc.date.available2011-07-29T08:57:10Z-
dc.date.issued2006-
dc.identifier.citationEuropean Journal of Immunology 36(6): 1374 - 1385, Jun 2006en_US
dc.identifier.issn0014-2980-
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/5677-
dc.descriptionThis article has been made available through the Brunel Open Access Publishing Fund and is available from the specified link - Copyright @ 2006 Wiley-Blackwell.en_US
dc.description.abstractRepetitive antigen stimulation induces peripheral T cell tolerance in vivo. It is not known, however, whether multiple stimulations merely suppress T cell activation or, alternatively, change the transcriptional program to a distinct, tolerant state. In this study, we have discovered that STAT3 and STAT5 were activated in response to antigen stimulation in vivo, in marked contrast to the suppression of AP-1, NF-kappaB and NFAT. In addition, a number of transcription factors were induced in tolerant T cells following antigen challenge in vivo, including T-bet, Irf-1 and Egr-2. The altered transcription program in tolerant cells associates closely with the suppression of cell cycle progression and IL-2 production, as well as with the induction of IL-10. Studies of T-bet and Egr-2 show that the function of T-bet in peptide treatment-induced regulatory T cells is not associated with Th1 differentiation, but correlates with the suppression of IL-2, whereas expression of Egr-2 led to an up-regulation of the cell cycle inhibitors p21(cip1) and p27(kip). Our results demonstrate a balanced transcription program regulated by different transcription factors for T cell activation and/or tolerance during antigen-induced T cell responses. Persistent antigen stimulation can induce T cell tolerance by changing the balance of transcription factors.en_US
dc.description.sponsorshipThis work was supported by a Programme Grant from the Wellcome Trust, Swedish Strategic Research fund, Barts Foundation for Research Limited and Brunel University.en_US
dc.languageeng-
dc.language.isoenen_US
dc.publisherWiley-Blackwellen_US
dc.subjectAnimalsen_US
dc.subjectCell cycleen_US
dc.subjectCell nucleusen_US
dc.subjectCyclin-dependent kinase inhibitor p21en_US
dc.subjectCyclin-dependent kinase inhibitor p27en_US
dc.subjectEarly growth response protein 2en_US
dc.subjectEpitopes, T-Lymphocyteen_US
dc.subjectGene expression profilingen_US
dc.subjectGene expression regulationen_US
dc.subjectImmune toleranceen_US
dc.subjectInterleukin-2en_US
dc.subjectLymphocyte activationen_US
dc.subjectMiceen_US
dc.subjectMice, transgenicen_US
dc.subjectOligonucleotide array sequence analysisen_US
dc.subjectRNAen_US
dc.subjectReverse transcriptase polymerase chain reactionen_US
dc.subjectSignal transductionen_US
dc.subjectT-box domain proteinsen_US
dc.subjectT-Lymphocytes, Regulatoryen_US
dc.subjectTranscription factorsen_US
dc.subjectTranscription, Geneticen_US
dc.subjectTransfectionen_US
dc.titlePersistent antigenic stimulation alters the transcription program in T cells, resulting in antigen-specific tolerance.en_US
dc.typeResearch Paperen_US
dc.identifier.doihttp://dx.doi.org/10.1002/eji.200635883-
pubs.organisational-data/Brunel-
pubs.organisational-data/Brunel/Brunel (Active)-
pubs.organisational-data/Brunel/Brunel (Active)/School of Health Science & Social Care-
pubs.organisational-data/Brunel/Research Centres-
pubs.organisational-data/Brunel/Research Centres/BICGP-
pubs.organisational-data/Brunel/School of Health Sciences and Social Care-
pubs.organisational-data/Brunel/School of Health Sciences and Social Care/BICGP-
Appears in Collections:Biological Sciences
Publications
Dept of Life Sciences Research Papers

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