Sjögren's syndrome (SjS) is a systemic autoimmune disease marked by xerostomia (dry mouth), keratoconjunctivitis sicca (eye dryness), and other systematic disorders. Its pathogenesis involves an inflammatory process that is characterized by lymphocytic infiltration into exocrine glands and other tissues. Although the development of ectopic lymphoid tissue and overproduction of autoantibodies by hyperactive B cells suggest that they may promote SjS development, treatment directed towards them fails to induce significant laboratory or clinical improvement. T cells are overwhelming infiltrators in most phases of the disease, and the involvement of multiple T cell subsets of suggests the extraordinary complexity of SjS pathogenesis. The factors, including various cellular subtypes and molecules, regulate the activation and suppression of T cells. T cell activation induces inflammatory cell infiltration, B cell activation, tissue damage, and metabolic changes in SjS. Knowledge of the pathways that link these T cell subtypes and regulation of their activities are not completely understood. This review comprehensively summarizes the research progress and our understanding of T cells in SjS, including CD4+ T cells, CD8+ TRM cells, and innate T cells, to provide insights into for clinical treatment.

中文翻译：

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干燥综合征 T 细胞的免疫生物学。

干燥综合征 (SjS) 是一种全身性自身免疫性疾病，以口干症（口干）、干燥性角结膜炎（眼干）和其他全身性疾病为特征。其发病机制涉及以淋巴细胞浸润到外分泌腺和其他组织为特征的炎症过程。尽管异位淋巴组织的发育和过度活跃的 B 细胞自身抗体的过度产生表明它们可能促进 SjS 的发展，但针对它们的治疗未能诱导显着的实验室或临床改善。在疾病的大多数阶段，T 细胞是压倒性的浸润者，并且多个 T 细胞亚群的参与表明 SjS 发病机制非常复杂。这些因子，包括各种细胞亚型和分子，调节 T 细胞的激活和抑制。T 细胞活化诱导炎性细胞浸润、B 细胞活化、组织损伤和 SjS 的代谢变化。尚未完全了解将这些 T 细胞亚型联系起来的途径及其活动的调节。本综述全面总结了SjS中T细胞的研究进展和我们对CD4+ T细胞、CD8+ TRM细胞和先天性T细胞的理解，以期为临床治疗提供见解。