Th17/Treg细胞的功能平衡是控制机体免疫稳态的关键环节，其平衡紊乱与多种炎症性疾病密切相关。表观遗传学修饰在免疫应答及调控过程中发挥重要作用，而其在T细胞免疫中的作用及机制尚不明确。我们前期发现了组蛋白甲基化转移酶Setd2在抗病毒天然免疫反应中的重要作用，而Setd2在适应性免疫应答中的功能仍不清楚。预实验表明Setd2在Th17/Treg细胞分化过程中差异表达，Setd2的CD4条件性敲除小鼠外周Treg细胞比例以及TGF-β触发的Smad3磷酸化水平明显下降，提示Setd2与T细胞功能调控有着重要关联。基于此，本项目将深入探讨Setd2分子对Th17/Treg细胞平衡的影响及机制，及其在T细胞介导的炎症性疾病中的调控作用。本项目将从表观遗传调控的角度揭示Th17/Treg细胞分化平衡及免疫调节的分子机制，并为炎症性疾病的发病机制研究及临床干预提供依据。

The immune balance mediated by Th17 and regulatory T (Treg) cells is critical for the maintenance of immune homeostasis. Disruption of Th17/Treg cell balance is closely associated with multiple inflammatory diseases. Epigenetic enzymes play essential roles in immune responses, yet its function in the development and function of T cells remains to be identified. We previously demonstrated that histone methyltransferase Setd2 is essential for amplifying antiviral innate immunity, however, the role of Setd2 in regulation of adaptive immunity remains unclear. Our preliminary study showed that Setd2 is differentially expressed during Th17 and Treg cell differentiation, and the mice with CD4 conditional knockout of Setd2 exhibited lower peripheral Treg cell proportion and impaired Smad3 phosphorylation triggered by TGF-beta. In this project, we aim to investigate the role of Setd2 in the balance of Th17 and Treg cell development and function, clarify its underlying molecular mechanisms, and also reveal the involvement of Setd2 in the pathogenesis of T cell-mediated inflammatory diseases. The project will shed new light on the molecular mechanisms of Th17/Treg cell balance and immune regulation, and provide novel target for the prevention and treatment of inflammatory diseases.