Xu Xuan, Zhou Jingying, Xie Haihua, Zhang Ruhan, Gu Bowen, Liu Li, Liu Mi, Chang Xiaorong
School of Acupuncture & Tuina and Rehabilitation, Hunan University of Chinese Medicine, Changsha, China.
The First Affiliated Hospital, Hunan University of Chinese Medicine, Changsha, China.
Front Immunol. 2025 Jul 7;16:1610254. doi: 10.3389/fimmu.2025.1610254. eCollection 2025.
Rheumatoid arthritis (RA) is an autoimmune disease, in which the abnormal activation and proliferation of effector T cells play a pivotal role in its pathogenesis. Regulatory T cells (Tregs) are a unique subset of immune cells with immunosuppressive functions, which help to inhibit the differentiation and proliferation of effector T cells in RA and maintain immune tolerance. The interaction between gut microbiota and immune cells has long been a research hotspot in autoimmune diseases. Although gut microbiota metabolites are considered to regulate the host's immune system as a bridge of the gut-joint axis, how gut microbiota acts on immunosuppressive Tregs remains unclear. This review summarizes that how the gut microbiota directly or indirectly (via metabolites) enhances the immunosuppressive capacity of Tregs. This enhancement is primarily achieved through pathways such as promoting the induction of Tregs, upregulating the expression of characteristic transcription factors of Tregs, and facilitating their secretion of anti-inflammatory cytokines, thereby ameliorating the inflammatory microenvironment and subsequently improving autoimmune conditions in RA.
类风湿关节炎（RA）是一种自身免疫性疾病，其中效应T细胞的异常激活和增殖在其发病机制中起关键作用。调节性T细胞（Tregs）是具有免疫抑制功能的独特免疫细胞亚群，有助于抑制RA中效应T细胞的分化和增殖并维持免疫耐受。肠道微生物群与免疫细胞之间的相互作用长期以来一直是自身免疫性疾病的研究热点。尽管肠道微生物群代谢产物被认为作为肠-关节轴的桥梁调节宿主免疫系统，但肠道微生物群如何作用于免疫抑制性Tregs仍不清楚。本综述总结了肠道微生物群如何直接或间接（通过代谢产物）增强Tregs的免疫抑制能力。这种增强主要通过促进Tregs的诱导、上调Tregs特征性转录因子的表达以及促进其抗炎细胞因子的分泌等途径实现，从而改善炎症微环境并随后改善RA中的自身免疫状况。
