T_H17 cells exemplify environmental immune adaptation: they can acquire both a pathogenic and an anti-inflammatory fate. However, it is not known whether the anti-inflammatory fate is merely a vestigial trait, or whether it serves to preserve the integrity of the host tissues. Here we show that the capacity of T_H17 cells to acquire an anti-inflammatory fate is necessary to sustain immunological tolerance, yet it impairs immune protection against S. aureus. Additionally, we find that TGF-β signalling via Smad3/Smad4 is sufficient for the expression of the anti-inflammatory cytokine, IL-10, in T_H17 cells. Our data thus indicate a key function of T_H17 cell plasticity in maintaining immune homeostasis, and dissect the molecular mechanisms explaining the functional flexibility of T_H17 cells with regard to environmental changes.

T _H 17 细胞是环境免疫适应的例证：它们可以获得致病性和抗炎性两种命运。然而，尚不清楚抗炎作用是否仅仅是一种退化特征，或者它是否有助于保持宿主组织的完整性。在这里，我们表明 T _H 17 细胞获得抗炎命运的能力是维持免疫耐受所必需的，但它会损害对S 的免疫保护。金黄色葡萄球菌。此外，我们发现通过 Smad3/Smad4 的 TGF-β 信号传导足以在 T _H 17 细胞中表达抗炎细胞因子 IL-10 。因此，我们的数据表明 T _{H 的}一个关键功能17 细胞在维持免疫稳态方面的可塑性，并剖析解释 T _H 17 细胞在环境变化方面的功能灵活性的分子机制。