Yao Yu-Feng, Wang Mei-Ying, Dou Xiao-Yan
Department of Ophthalmology, Shenzhen Second People's Hospital, the First Affiliated Hospital of Shenzhen University, Shenzhen 518035, Guangdong Province, China.
Shantou University Medical College, Shantou 515031, Guangdong Province, China.
Int J Ophthalmol. 2022 Nov 18;15(11):1864-1872. doi: 10.18240/ijo.2022.11.19. eCollection 2022.
The recognition of the profound impact of the human gastrointestinal microbiome (GM) on human autoimmune diseases has gradually increased thanks to deeper research efforts. As a systemic autoimmune disease, primary Sjögren's syndrome (pSS) cannot be completely cured. Human studies have revealed that GM species and diversity are altered in patients with pSS compared with healthy individuals. Animal studies have provided possible mechanisms for the association between pSS and GM. The potential role of GM in pSS is exerted through several mechanisms. GM dysbiosis leads to increased intestinal permeability, which increases the risk of GM antigen exposure and activates specific autoreactive T lymphocytes "molecular mimicry". In addition, GM antigen exposure and intestinal immune tolerance loss caused by GM dysbiosis together induce chronic local gut mucosal inflammation, which deteriorates to systemic chronic non-specific inflammation with the circulation of pro-inflammatory lymphocytes and cytokines. These factors eventually activate autoreactive B lymphocytes and lead to pSS. If GM plays a key role in the pathogenesis of pSS, clarifying the underlying mechanisms will be helpful for the development of new therapies targeting GM for dry eye associated with pSS. This review summarizes the latest knowledge about the relationship between GM and pSS, with the aim of contributing to future research and to the development of new clinical applications.
随着研究的不断深入,人们逐渐认识到人类胃肠道微生物群(GM)对人类自身免疫性疾病有着深远影响。作为一种系统性自身免疫性疾病,原发性干燥综合征(pSS)无法完全治愈。人体研究表明,与健康个体相比,pSS患者的GM种类和多样性发生了改变。动物研究为pSS与GM之间的关联提供了可能的机制。GM在pSS中的潜在作用是通过多种机制发挥的。GM失调导致肠道通透性增加,从而增加了GM抗原暴露的风险,并激活特定的自身反应性T淋巴细胞,即“分子模拟”。此外,GM失调引起的GM抗原暴露和肠道免疫耐受丧失共同诱导慢性局部肠道黏膜炎症,随着促炎淋巴细胞和细胞因子的循环,炎症恶化为全身性慢性非特异性炎症。这些因素最终激活自身反应性B淋巴细胞,导致pSS。如果GM在pSS的发病机制中起关键作用,阐明其潜在机制将有助于开发针对与pSS相关的干眼症的新型GM靶向疗法。本综述总结了关于GM与pSS关系的最新知识,旨在为未来的研究和新临床应用的开发做出贡献。