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Comprehensive TCR repertoire analysis of CD4+ T-cell subsets in rheumatoid arthritis. 2020
Xu Jiang, and
Shiyu Wang, and
Chen Zhou, and
Jinghua Wu, and
Yuhao Jiao, and
Liya Lin, and
Xin Lu, and
Bo Yang, and
Wei Zhang, and
Xinyue Xiao, and
Yueting Li, and
Xunyao Wu, and
Xie Wang, and
Hua Chen, and
Lidan Zhao, and
Yunyun Fei, and
Huaxia Yang, and
Wen Zhang, and
Fengchun Zhang, and
Hui Chen, and
Jianmin Zhang, and
Bin Li, and
Huanming Yang, and
Jian Wang, and
Xiao Liu, and
Xuan Zhang
Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Clinical Immunology Center, Chinese Academy of Medical Sciences and Peking Union Medical College; The Ministry of Education Key Laboratory, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, 100730, China.
The pathogenesis of rheumatoid arthritis (RA), a systemic autoimmune disease characterized by autoreactive T-cell accumulation and pro-inflammatory cytokine overproduction, is unclear. Systematically addressing T-cell receptor (TCR) repertoires of different CD4+ T-cell subsets could help understand RA pathogenesis. Here, peripheral CD4+ T cells from treatment-naïve RA patients and healthy controls were sorted into seven subsets including naïve, effector, central memory, effector memory (EMT), Th1, Th17, and regulatory T cells. T-cell receptor β chain repertoires were then analyzed by next-generation sequencing. We identified T-cell clonal expansion in EMT and Th17 cells of RA patients, with highly similar TCR repertoires. Ex vivo experiments demonstrated the preferred differentiation from EMT to Th17 cells in RA. Notably, we showed that TCR diversity and abundance of differentiated T cells of Th17 were significantly correlated with RA disease activity. Based on these observations, we propose that abnormal differentiation from EMT to Th17 and expansion of Th17 play pivotal role in RA pathogenesis.
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