The discovery of forkhead box p3 (Foxp3) as the critical transcriptional controller of suppressive function in murine CD4(+) T regulatory (Treg) cells has allowed precise analyses of these cells in a range of immunopathological models. Recent data have revealed key roles for Foxp3+ Tregs in murine models of human organ-specific autoimmune conditions. Do these Tregs target the same autoantigens recognized by the autoaggressive T cells that need to be controlled? Under steady state conditions there may not be a need for such a shared recognition to dampen spontaneous anti-self priming in the lymphoid organs. However, when they are needed to control ongoing inflammation, Tregs recognizing autoantigens found in the diseased organ appear to have significantly stronger suppressive powers. We reflect on these observations that clearly have relevance for the translation of Treg-targeting immune therapies to human disease.

中文翻译：

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自身攻击的多方面控制：器官特异性自身免疫疾病小鼠模型中的 Foxp3+ 调节性 T 细胞。

叉头盒 p3 (Foxp3) 作为鼠 CD4(+) T 调节 (Treg) 细胞中抑制功能的关键转录控制器的发现允许在一系列免疫病理模型中对这些细胞进行精确分析。最近的数据揭示了 Foxp3+ Tregs 在人类器官特异性自身免疫疾病的小鼠模型中的关键作用。这些 Treg 是否针对需要控制的自身攻击性 T 细胞识别的相同自身抗原？在稳态条件下，可能不需要这种共同识别来抑制淋巴器官中的自发性反自启动。然而，当需要它们来控制持续的炎症时，识别患病器官中发现的自身抗原的 Treg 似乎具有明显更强的抑制能力。