发病机制
过继性细胞移植
CD8型
T细胞
医学
淋巴
免疫学
自身免疫
自身抗体
抗体
免疫系统
病理
作者
Xiang Lin,Jie Tian,Ke Rui,Kongyang Ma,King‐Hung Ko,Shengjun Wang,Liwei Lu
标识
DOI:10.1136/annrheumdis-2014-205521
摘要
We thank Alunno et al for their interest in our recently published work and their insightful comments regarding the roles of T helper (Th) 17 cell subsets during the pathogenesis of Sjogren's syndrome (SS) in mouse model and humans.1
In our study, we characterised the kinetic changes of IL-17-producing CD4 Th17 cells in salivary glands (SG) and draining cervical lymph nodes (CLN), and examined their correlations with clinical, histological and serological features of SS in mice immunised with SG proteins. Moreover, we revealed that IL-17 knockout (KO) mice were completely resistant for SS induction, while adoptive transfer of Th17 cells rapidly induced a full profile of SS in immunised IL-17 KO mice with markedly reduced saliva secretion, elevated autoantibody production and pronounced lymphocytic inflammation and tissue damage in SG. Together, our findings have defined a critical role of Th17 cells in the pathogenesis of SS in mice. Recently, there is increasing evidence indicating the involvement of several IL-17-producing T cell subsets in the development of SS in humans and mouse.2–4 In particular, an increased IL-17-producing T cell subset lacking CD4 and CD8 surface molecules (double negative, DN) was found in the peripheral blood …
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