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TCR repertoire analysis reveals effector memory T cells differentiation into Th17 cells in rheumatoid arthritis

By Xu Jiang, Shi-yu Wang, Chen Zhou, Jing-hua Wu, Yu-hao Jiao, Li-ya Lin, Xin Lu, Bo Yang, Wei Zhang, Xin-yue Xiao, Yue-ting Li, Xun-yao Wu, Xie Wang, Yiming Bao, Li-dan Zhao, Yun-yun Fei, Hua-xia Yang, Wen Zhang, Feng-chun Zhang, Hui Chen, Jian-min Zhang, Bin Li, Huan-ming Yang, Jian Wang, Wei A He, Xue-tao Cao, De-pei Liu, Xiao Liu, Xuan Zhang

Posted 23 Apr 2019
bioRxiv DOI: 10.1101/616441

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-naive RA patients and healthy controls were sorted into seven subsets including naive, effector, central memory, effector memory (EMT), Th1, Th17, and regulatory T cells. T-cell receptor beta chain repertoires were then analyzed by next-generation sequencing. We identified T-cell clonal expansion in EMT and Th17 cells, with highly similar TCR repertoires between them. Ex vivo experiments demonstrated the preferred differentiation from EMT to Th17 cells in RA. Moreover, TCR diversity in subsets including Th17 was negatively correlated with RA disease activity indices such as C-reactive protein and erythrocyte sedimentation rate. Thus, shared and abnormally expanded EMT and Th17 TCR repertoires might be pivotal for RA pathogenesis.

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