Despite the cellular heterogeneity of IL-6RhiTIGIT− mTregs, our findings have important implications for the clinical studies exploring the expansion of CD4+ CD127lowCD25+ T cells for the treatment of autoimmune diseases, and identify a population of IL-6RhiTIGIT− T cells within this compartment containing a significant fraction of activated effector Tregs, which likely mediate their suppression in part by IL-10 production [65] and CTLA-4 binding to the co-stimulatory molecules CD80 and CD86 [66], [67]. This evidence concerns the gene CD86 and autoimmune disease.