Interleukin-7 is required for CD4(+) T cell activation and autoimmune neuroinflammation.
Interleukin-7 is required for CD4(+) T cell activation and autoimmune neuroinflammation.
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DOI：
10.1016/j.clim.2015.08.007
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发表时间：
2015-12
期刊：
影响因子：
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通讯作者：
Theofilopoulos AN
中科院分区：
文献类型：
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作者：
Lawson BR;Gonzalez-Quintial R;Eleftheriadis T;Farrar MA;Miller SD;Sauer K;McGavern DB;Kono DH;Baccala R;Theofilopoulos AN
已知IL-7对于T细胞稳态是至关重要的，但先前已假定其对于TCR诱导的活化是不可或缺的。在这里，我们发现IL-7对于CD 4 + T细胞的初始活化至关重要，因为它提供了一些必要的早期信号传导成分，如活化的STAT 5和Akt。因此，短期体内IL-7 R α阻断可抑制自身抗原特异性CD 4 + T细胞的活化和扩增，当用于治疗实验性自身免疫性脑脊髓炎（EAE）时，可预防和改善疾病。我们的研究表明，IL-7信号传导是最佳CD 4 + T细胞活化的先决条件，IL-7 R拮抗作用可能有效治疗CD 4 + T细胞介导的神经炎症和其他自身免疫性炎症。
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-7Rα 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.