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PDLIM2 restricts Th1 and Th17 differentiation and prevents autoimmune disease

DOI: 10.1186/2045-3701-2-23

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Abstract:

Here we report that naive PDLIM2 deficient CD4+ T cells were prone to differentiate into Th1 and Th17 cells. PDLIM2 deficiency, however, had no obvious effect on lineage commitment towards Th2 or Treg cells. Notably, PDLIM2 deficient mice exhibited increased susceptibility to experimental autoimmune encephalitis (EAE), a Th1 and/or Th17 cell-mediated inflammatory disease model of multiple sclerosis (MS). Mechanistic studies further indicate that PDLIM2 was required for restricting expression of Th1 and Th17 cytokines, which was in accordance with the role of PDLIM2 in the termination of NF-κB and STAT activation.These findings suggest that PDLIM2 is a key modulator of T-cell-mediated immune responses that may be targeted for the therapy of human autoimmune diseases.CD4+ T helper (Th) cells play a central role in orchestrating immune responses to diverse microbial pathogens [1]. Upon activation by antigens, naive CD4+ T cells differentiate into specialized effector T (Teff) cells (Th1, Th2, or Th17), which secrete different patterns of cytokines and perform different functions [1]. Th1 cells produce interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) and initiate cellular immune responses against intracellular pathogens. Th2 cells generate interleukin-4 (IL-4), IL-5 and IL-13 and promote humoral responses against extracellular parasites. Th17 cells make IL-17, IL-21 and IL-22 and confer immunity against extracellular bacteria and fungi. Moreover, activated CD4+ T cells also differentiate into regulatory T (Treg) cells, which express transforming growth factor-β (TGF-β), IL-10 and IL-35 and suppress the functions of Teff cells, thereby keeping immune responses in check.Imbalance of Th cell differentiation and subsequent cytokine dysregulation is implicated in inflammatory and autoimmune diseases [2]. In particular, Th1 and Th17 cells and their signature cytokines IFN-γ and IL-17 have been shown to play a critical role in the development of autoimmune responses in

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