Sjögren syndrome (SS) is a chronic autoimmune disorder that primarily targets the salivary and lacrimal glands. The pathology of these exocrine glands is characterized by periductal focal lymphocytic infiltrates, and both T cell-mediated tissue injury and autoantibodies that interfere with the secretion process underlie glandular hypofunction. In addition to these adaptive mechanisms, multiple innate immune pathways are dysregulated, particularly in the salivary gland epithelium. Our understanding of the pathogenetic mechanisms of SS has substantially improved during the past decade. In contrast to viral infection, bacterial infection has never been considered in the pathogenesis of SS. In this review, oral dysbiosis associated with SS and evidence for bacterial infection of the salivary glands in SS were reviewed. In addition, the potential contributions of bacterial infection to innate activation of ductal epithelial cells, plasmacytoid dendritic cells, and B cells and to the breach of tolerance via bystander activation of autoreactive T cells and molecular mimicry were discussed. The added roles of bacteria may extend our understanding of the pathogenetic mechanisms and therapeutic approaches for this autoimmune exocrinopathy.

中文翻译：

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为什么我们应该考虑口腔细菌在干燥综合征发病机制中的潜在作用？

干燥综合征 (SS) 是一种慢性自身免疫性疾病，主要针对唾液腺和泪腺。这些外分泌腺的病理学特征是导管周围局灶性淋巴细胞浸润，T 细胞介导的组织损伤和干扰分泌过程的自身抗体是腺体功能减退的基础。除了这些适应性机制外，多种先天免疫通路失调，特别是在唾液腺上皮细胞中。在过去的十年中，我们对 SS 发病机制的理解有了很大的提高。与病毒感染相比，SS 的发病机制中从未考虑过细菌感染。在这篇综述中，回顾了与 SS 相关的口腔生态失调和 SS 中唾液腺细菌感染的证据。此外，讨论了细菌感染对导管上皮细胞、浆细胞样树突状细胞和 B 细胞的先天激活以及通过旁观者激活自身反应性 T 细胞和分子模拟而破坏耐受的潜在贡献。细菌的附加作用可能会扩展我们对这种自身免疫性外分泌病的发病机制和治疗方法的理解。