Regulatory T cells (Tregs) play a critical role in regulating tissue inflammation. Reduced Treg numbers and/or suppressive function contribute to autoimmune disease. Tregs can adopt the transcriptional programming of T helper (Th) type-1/2/17 cells to optimally suppress these subsets. Under specific conditions, these Th-like Tregs lose suppressive capacity and release proinflammatory cytokines to promote inflammation. This Treg plasticity depends on inflammatory mediators in the local environment. In this study, we review how cytokines impact Treg function and may contribute to autoimmune disease. A comprehensive understanding of Th-like Tregs may elucidate novel and more focused therapeutic approaches.
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