Opposing Roles for RelB and Bcl-3 in Regulation of T-Box Expressed in T Cells, GATA-3, and Th Effector Differentiation
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چکیده
منابع مشابه
Opposing roles for RelB and Bcl-3 in regulation of T-box expressed in T cells, GATA-3, and Th effector differentiation.
CD4+ T cells with a block in the NF-kappaB signaling pathway exhibit decreases in Th1 responses and diminished nuclear levels of multiple transactivating NF-kappaB/Rel/IkappaB proteins. To determine the lineage-intrinsic contributions of these transactivators to Th differentiation, T cells from mice deficient in specific subunits were cultured in exogenous cytokines promoting either Th1 or Th2 ...
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Objective(s): Multiple sclerosis (MS) is considered as a chronic type of an inflammatory disease characterized by loss of myelin of CNS.Recent evidence indicates that Interleukin 17 (IL-17)-producing T helper cells (Th17 cells) population are increased and regulatory T cells (Treg cells) are decreased in MS. Despite extensive research in understanding the mechanism of Th17 and Treg differentiat...
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Introduction: Multiple Sclerosis (MS) is an inflammatory disorder caused by self-reactive Th1 lymphocytes, while Th2 cells may confer protection. The Th1 and Th2 cell differentiation are regulated by specific transcription factors, especially T-bet and GATA-3, respectively. This investigation aimed to measure the T-bet and GATA-3 expression by Peripheral Blood Mononuclear Cells (PBMCs) obtained...
متن کاملEffector/memory CD4 T cells making either Th1 or Th2 cytokines commonly co-express T-bet and GATA-3
Naïve CD4 T (NCD4T) cells post-activation undergo programming for inducible production of cytokines leading to generation of memory cells with various functions. Based on cytokine based polarization of NCD4T cells in vitro, programming for either 'Th1' (interferon-gamma [IFNg]) or 'Th2' (interleukin [IL]-4/5/13) cytokines is thought to occur via mutually exclusive expression and functioning of ...
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ژورنال
عنوان ژورنال: The Journal of Immunology
سال: 2005
ISSN: 0022-1767,1550-6606
DOI: 10.4049/jimmunol.175.4.2102