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Interleukin-7 is required for CD4(+) T cell activation and autoimmune neuroinflammation

机译:CD4(+)T细胞激活和自身免疫性神经炎症需要白细胞介素7

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摘要

IL-7 is known to be vital for T cell homeostasis but has previously been presumed to be dispensable for TCR-induced activation. Here, we show that IL-7 is critical for the initial activation of CD4(+) T cells in that it provides some of the necessary early signaling components, such as activated STAT5 and Akt. Accordingly, short-term in vivo IL-7R alpha blockade inhibited the activation and expansion of autoantigen-specific CD4(+) T cells and, when used to treat experimental autoimmune encephalomyelitis (EAE), prevented and ameliorated disease. Our studies demonstrate that IL-7 signaling is a prerequisite for optimal CD4(+) T cell activation and that IL-7R antagonism may be effective in treating CD4(+) T cell-mediated neuroinflammation and other autoimmune inflammatory conditions. (C) 2015 Elsevier Inc. All rights reserved.
机译:众所周知,IL-7对于T细胞稳态至关重要,但先前被认为对于TCR诱导的激活是不可或缺的。在这里,我们显示IL-7对于CD4(+)T细胞的初始激活至关重要,因为它提供了一些必要的早期信号传导成分,例如激活的STAT5和Akt。因此,短期的体内IL-7Rα阻断作用抑制了自身抗原特异性CD4(+)T细胞的活化和扩增,并且在用于治疗实验性自身免疫性脑脊髓炎(EAE)时,可以预防和改善疾病。我们的研究表明,IL-7信号传导是CD4(+)T细胞最佳活化的前提,并且IL-7R拮抗作用可能有效治疗CD4(+)T细胞介导的神经炎症和其他自身免疫性炎症。 (C)2015 Elsevier Inc.保留所有权利。

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