免疫学
失调
肠道菌群
类风湿性关节炎
微生物群
自身免疫
分子模拟
医学
串扰
免疫系统
发病机制
免疫
粘膜免疫
自身免疫性疾病
粘膜免疫学
生物
益生菌
肠道微生物群
关节炎
滑膜炎
粪便细菌疗法
塞库金单抗
来氟米特
白细胞介素23
CTLA-4号机组
炎症性肠病
溃疡性结肠炎
补体系统
炎症
敏化
脱敏(药物)
移植
作者
Yang Yun,Guoqiang Xu,Xiaojing Jiang,Xiubao Ren,Min‐Chi Lu,Junwei Chen,Sheng‐Xiao Zhang
摘要
Rheumatoid arthritis (RA), a chronic autoimmune disorder driven by genetic-environmental interplay, manifests as progressive synovitis and irreversible joint damage. Despite mechanistic advances in disease-modifying antirheumatic drugs (DMARDs) and biologics, upstream mucosal triggers of autoimmunity remain elusive. Mounting evidence implicates gut microbiota dysbiosis as a pivotal environmental factor in RA pathogenesis through multifaceted mechanisms: (1) compromising intestinal barrier integrity, (2) facilitating molecular mimicry via cross-reactive microbial antigens, (3) skewing mucosal immunity toward pro-inflammatory T helper 17 (Th17)/T follicular helper (Tfh) cell responses, and (4) generating bioactive metabolites with dual roles in regulating osteoclastogenesis and synovial inflammation. This review synthesizes recent advances in gut microbiome profiling, mechanistic studies, and preclinical models, elucidating microbial-host crosstalk in autoimmune cascades. Furthermore, we critically evaluate microbiota-directed strategies, including dietary and probiotic modulation, microbiome-informed optimization of conventional DMARDs and biologics, and investigational approaches like fecal microbiota transplantation and Chinese herbal medicine, that may offer promising adjunctive approaches to complement conventional RA management.
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