Guanghua Clinical Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Department of Rheumatology, Shanghai Guanghua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Front Immunol. 2022 Mar 3;13:863703. doi: 10.3389/fimmu.2022.863703. eCollection 2022.
Rheumatoid arthritis (RA) is an autoimmune disease that can cause joint damage and disability. Epigenetic variation, especially DNA methylation, has been shown to be involved in almost all the stages of the pathology of RA, from autoantibody production to various self-effector T cells and the defects of protective T cells that can lead to chronic inflammation and erosion of bones and joints. Given the critical role of T cells in the pathology of RA, the regulatory functions of DNA methylation in T cell biology remain unclear. In this review, we elaborate on the relationship between RA pathogenesis and DNA methylation in the context of different T cell populations. We summarize the relevant methylation events in T cell development, differentiation, and T cell-related genes in disease prediction and drug efficacy. Understanding the epigenetic regulation of T cells has the potential to profoundly translate preclinical results into clinical practice and provide a framework for the development of novel, individualized RA therapeutics.
类风湿关节炎（RA）是一种自身免疫性疾病，可导致关节损伤和残疾。表观遗传变异，特别是 DNA 甲基化，已被证明参与 RA 病理学的几乎所有阶段，从自身抗体产生到各种自身效应 T 细胞和保护性 T 细胞的缺陷，这些缺陷可导致慢性炎症和骨骼关节侵蚀。鉴于 T 细胞在 RA 发病机制中的关键作用，DNA 甲基化在 T 细胞生物学中的调节功能仍不清楚。在这篇综述中，我们详细阐述了不同 T 细胞群中 RA 发病机制与 DNA 甲基化之间的关系。我们总结了 T 细胞发育、分化以及疾病预测和药物疗效相关 T 细胞基因中的相关甲基化事件。了解 T 细胞的表观遗传调控有可能将临床前研究结果深刻转化为临床实践，并为开发新的、个体化的 RA 治疗方法提供框架。
