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Reciprocal developmental pathways for the generation of pathogenic effector T(H)17 and regulatory T cells

机译：病原性效应T（H）17和调节性T细胞生成的相互发展途径

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On activation, T cells undergo distinct developmental pathways, attaining specialized properties and effector functions. T-helper (T-H) cells are traditionally thought to differentiate into T(H)1 and T(H)2 cell subsets. T(H)1 cells are necessary to clear intracellular pathogens and T(H)2 cells are important for clearing extracellular organisms(1,2). Recently, a subset of interleukin ( IL)-17-producing T (T(H)17) cells distinct from T(H)1 or T(H)2 cells has been described and shown to have a crucial role in the induction of autoimmune tissue injury(3-5). In contrast, CD4(+) CD25(+) Foxp3(+) regulatory T (T-reg) cells inhibit autoimmunity and protect against tissue injury(6). Transforming growth factor-beta (TGF-beta) is a critical differentiation factor for the generation of T-reg cells(7). Here we show, using mice with a reporter introduced into the endogenous Foxp3 locus, that IL-6, an acute phase protein induced during inflammation(8,9), completely inhibits the generation of Foxp3(+) T-reg cells induced by TGF-beta. We also demonstrate that IL-23 is not the differentiation factor for the generation of T(H)17 cells. Instead, IL-6 and TGF-beta together induce the differentiation of pathogenic T(H)17 cells from naive T cells. Our data demonstrate a dichotomy in the generation of pathogenic (T(H)17) T cells that induce autoimmunity and regulatory (Foxp3(+)) T cells that inhibit autoimmune tissue injury.
机译：激活后，T细胞经历不同的发育途径，获得专门的特性和效应子功能。传统上认为T辅助（T-H）细胞可以分化为T（H）1和T（H）2细胞子集。 T（H）1细胞对于清除细胞内病原体是必不可少的，而T（H）2细胞对于清除细胞外生物很重要（1,2）。最近，已描述了不同于T（H）1或T（H）2细胞的产生白介素（IL）-17的T（T（H）17）细胞的子集，并显示了在诱导白细胞介素（IL）-17中起关键作用自身免疫组织损伤（3-5）。相比之下，CD4（+）CD25（+）Foxp3（+）调节性T（T-reg）细胞抑制自身免疫并保护组织免受伤害（6）。转化生长因子-β（TGF-beta）是产生T-reg细胞的关键分化因子（7）。在这里，我们显示，使用将记者引入内源性Foxp3基因座的小鼠，炎症期间诱导的急性期蛋白IL-6（8,9）完全抑制了TGF诱导的Foxp3（+）T-reg细胞的生成-beta。我们还证明IL-23不是T（H）17细胞生成的分化因子。取而代之的是，IL-6和TGF-β共同诱导从原始T细胞分化出致病性T（H）17细胞。我们的数据表明，在诱导自身免疫性的致病性（T（H）17）T细胞和抑制自身免疫性组织损伤的调节性（Foxp3（+））T细胞的产生中存在分歧。

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