Fever has beneficial effects on immune responses; however, its impact on T cell polarization is poorly understood. In this issue of Immunity, Wang et al. show that fever acts through a T cell-intrinsic SMAD4-dependent mechanism that selectively drives Th17 cell differentiation and pathogenicity in autoimmunity.

中文翻译：

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发烧Th17细胞免疫轴：一些SMAD喜欢它。

发烧对免疫反应具有有益作用；然而，其对T细胞极化的影响知之甚少。在本期《免疫》中，Wang等人。研究表明发烧是通过T细胞内在的SMAD4依赖性机制起作用的，该机制选择性地驱动Th17细胞在自身免疫中的分化和致病性。