International journal of rheumatic diseases · 2024
CCR5 mediates rheumatoid arthritis progression by promoting the activation and proliferation of non-classical Th1 cells.
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Miao Jinlin, Zhang Bei, Sun Haoyang, Zhang Peiyan, Shen Haomiao, Wang Jiawei, Jia Junfeng, Zhang Kui, Zheng Zhaohui, Zhu Ping
Аннотация
AIM: Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by immune dysegulation, including an immune imbalance due to abnormal activation of non-classical Th1 cells (CD161+ Th1). This study investigated the effects of CCR5 on the activation and proliferation of CD161+ Th1 and their pathogenicity in patients with RA.
METHODS: The study was conducted on 53 patients with RA and 32 age- and sex-matched healthy controls (HC). The cell phenotype was assessed by flow cytometry and the cytokine levels in the supernatant were detected by ELISA.
RESULTS: We demonstrate a marked increase in CD161+ Th1 cells in the synovial fluid of RA patients. These cells exhibit a hyperactivated and hyperproliferative state alongside elevated CCR5 expression. Furthermore, the levels of CD161+ Th1 cells, CD25, and CCR5 in RA synovial fluid show a positive correlation with the disease activity. Additionally, our study reveals that CCR5 facilitates the activation, proliferation, and cytokine production of CD161+ Th1 cells through the pZAP70/NFAT signaling pathway.
CONCLUSION: These findings contribute to a deeper understanding of RA pathogenesis and uncover a novel mechanism that regulates non-classical CD161+ Th1 responses in RA, which may provide a potential therapeutic target.
METHODS: The study was conducted on 53 patients with RA and 32 age- and sex-matched healthy controls (HC). The cell phenotype was assessed by flow cytometry and the cytokine levels in the supernatant were detected by ELISA.
RESULTS: We demonstrate a marked increase in CD161+ Th1 cells in the synovial fluid of RA patients. These cells exhibit a hyperactivated and hyperproliferative state alongside elevated CCR5 expression. Furthermore, the levels of CD161+ Th1 cells, CD25, and CCR5 in RA synovial fluid show a positive correlation with the disease activity. Additionally, our study reveals that CCR5 facilitates the activation, proliferation, and cytokine production of CD161+ Th1 cells through the pZAP70/NFAT signaling pathway.
CONCLUSION: These findings contribute to a deeper understanding of RA pathogenesis and uncover a novel mechanism that regulates non-classical CD161+ Th1 responses in RA, which may provide a potential therapeutic target.