Th17 cells are implicated in the pathogenesis of numerous autoimmune diseases so strategies to inhibit their development and/or function are being developed. One approach involves inhibition of RORC2, the master transcription factor of Th17 cells, but how this strategy impacted other RORC2‐expressing T cells was unclear. In this issue, Boardman et al. demonstrate that RORC2 inhibition offers a dualaction approach to diminish undesired inflammatory responses. As well as dampening the activity of Th17 cells, thestudy shows that RORC2 inhibition simultaneously promotes the stability and function of human Tregs. Specifically, inflammatory‐cytokine‐induced instability of Th17‐like Tregs was ameliorated by RORC2 inhibition. Furthermore, inhibiting RORC2 in Th17‐like Tregs promoted secretion of the antiinflammatory cytokine IL‐10, thereby improving Tregmediated suppression of innate responses. Overall, these findings reveal a previously unknown, and therapeutically beneficial, side effect of RORC2 inhibition, and provide a further rationale for the continued development of RORC2 inhibitors for treating inflammatory disorders.

Th17细胞与多种自身免疫性疾病的发病机制有关，因此正在制定抑制其发展和/或功能的策略。一种方法涉及抑制Th17细胞的主要转录因子RORC2，但是尚不清楚该策略如何影响其他表达RORC2的T细胞。在本期中，Boardman等人。证明RORC2抑制提供了双重作用的方法，以减少不良的炎症反应。研究表明，除了抑制Th17细胞的活性外，RORC2抑制还可以促进人类Treg的稳定性和功能。特别是，通过RORC2抑制可减轻炎症细胞因子诱导的Th17样Treg的不稳定性。此外，抑制Th17样Treg中的RORC2可以促进抗炎细胞因子IL-10的分泌，从而改善Treg介导的先天反应抑制。总体而言，这些发现揭示了RORC2抑制的先前未知且对治疗有益的副作用，并为继续开发用于治疗炎症性疾病的RORC2抑制剂提供了进一步的理论依据。