Critical role of G protein-coupled receptor 40 in B cell response and the pathogenesis of rheumatoid arthritis in mice and patients

Rheumatoid arthritis (RA) is marked by joint damage and inflammation, with B cells playing a key role by generating autoantibodies. This study shows that G protein-coupled receptor 40 (GPR40) deficiency in B cells leads to increased activation, proliferation, antibody production, germinal center formation, and class switch recombination. GPR40 regulates Plcγ2 phosphorylation and intracellular calcium flux downstream of the B cell receptor by binding to the Gαq protein. In GPR40-deficient mice, susceptibility to collagen-induced arthritis was higher. GPR40 agonists showed potential as therapeutic agents, and their reduced expression in patients with RA correlated with disease onset, suggesting GPR40 as a potential therapeutic target and diagnostic marker.

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Publication Details

Journal
Cell Reports
Published
2024-10-01
DOI
https://doi.org/10.1016/j.celrep.2024.114858
Citations
3
Primary Topic
Chemokine receptors and signaling
Type
article
Field-Weighted Citation Impact
0.85

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article

Critical role of G protein-coupled receptor 40 in B cell response and the pathogenesis of rheumatoid arthritis in mice and patients

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Cell Reports
Chemokine receptors and signaling
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article

Critical role of G protein-coupled receptor 40 in B cell response and the pathogenesis of rheumatoid arthritis in mice and patients

Jing Li, Tao Sun, Lixia Huo, Yunliang Yao, Yanfeng Yi, Jiantong Shen, Anqi Li, Jue Wang, Xiaoyi Wang, Xiaoyu Li, Zhihong Wang, Yang Liu, Xiao-Bing Yang, Juanjie Wu, Jiapeng Gao, Jiexun Cai
article en
3 citations

Abstract

Rheumatoid arthritis (RA) is marked by joint damage and inflammation, with B cells playing a key role by generating autoantibodies. This study shows that G protein-coupled receptor 40 (GPR40) deficiency in B cells leads to increased activation, proliferation, antibody production, germinal center formation, and class switch recombination. GPR40 regulates Plcγ2 phosphorylation and intracellular calcium flux downstream of the B cell receptor by binding to the Gαq protein. In GPR40-deficient mice, susceptibility to collagen-induced arthritis was higher. GPR40 agonists showed potential as therapeutic agents, and their reduced expression in patients with RA correlated with disease onset, suggesting GPR40 as a potential therapeutic target and diagnostic marker.

Cell ReportsVol. 43(10)
Huzhou Normal University (CN), Soochow University (CN), Huzhou Central Hospital (CN)
National Natural Science Foundation of China, Zhejiang University, Huzhou Municipal Science and Technology Bureau, Natural Science Foundation of Zhejiang Province
Openalex Percentile: Top 22%
Chemokine receptors and signaling
0.85
DOIOpen Access PDFOpenAlex
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