Regulatory T cells (Tregs) are necessary to prevent autoimmune disease. As such, stable FoxP3 expression is required for the proper function of Tregs in the control of autoimmune disease. Different Treg subsets that utilize different mechanisms of suppression have been identified. The T-cell immunoglobulin immunoreceptor tyrosine-based inhibitory motif (TIGIT) is a relatively new Treg cell marker that has a suppressive function. We have previously identified the adenosine 2A receptor (A2Ar) as a requirement for the emergence of Tregs following resolution of autoimmune disease. Using a FoxP3-GFP-Cre reporter mouse, we identify FoxP3 and ‘exFoxP3’ cells, show FoxP3 and not exFoxP3 cells are suppressive. We further show FoxP3 cells express TIGIT, and are induced through A2Ar in healthy volunteers, but not patients with autoimmune disease. Furthermore, we show Tregs emerge in the target tissue at the onset of autoimmune disease in an A2Ar-dependent manner. In summary, we identify a novel subset of TIGIT⁺ Tregs that are induced through stimulation of the A2Ar.

调节性 T 细胞 (Tregs) 是预防自身免疫性疾病所必需的。因此，稳定的 FoxP3 表达是 Tregs 在控制自身免疫疾病中的正常功能所必需的。已经确定了利用不同抑制机制的不同 Treg 子集。T 细胞免疫球蛋白免疫受体酪氨酸抑制基序 (TIGIT) 是一种相对较新的 Treg 细胞标记物，具有抑制功能。我们之前已经确定腺苷 2A 受体 (A2Ar) 是自身免疫性疾病解决后 Treg 出现的必要条件。使用 FoxP3-GFP-Cre 报告小鼠，我们识别 FoxP3 和“exFoxP3”细胞，显示 FoxP3 而非 exFoxP3 细胞是抑制性的。我们进一步显示 FoxP3 细胞表达 TIGIT，并在健康志愿者中通过 A2Ar 诱导，但在自身免疫性疾病患者中则不然。此外，我们显示 Tregs 在自身免疫性疾病发作时以 A2Ar 依赖性方式出现在靶组织中。总之，我们确定了一个新的 TIGIT 子集⁺通过刺激 A2Ar 诱导的 Treg。