Recently, Ms. Li Anqi (first author), Professor Wang Xiaoyi (co-first author), and Professor Yao Yunliang (corresponding author) from the School of Medicine/Nursing and the First Affiliated Hospital of Huzhou University, with Huzhou University as the first unit, published a research article titled “Critical role of G protein-coupled receptor 40 in B cell response and the pathogenesis of rheumatoid arthritis in mice and patients” in the well-known sub-journal of Cell Cell Reports (TOP Q1 Chinese Academy of Sciences, IF:7.5). Relevant clinical teams from the First Affiliated Hospital, the Central Hospital Affiliated, and the Third People’s Hospital participated in the project research.

　　Rheumatoid arthritis (RA) is characterized by joint damage and inflammation.  B cells play a crucial role by producing autoantibodies to defend against this disease. In this study, the author team found that the deficiency of G protein-coupled receptor 40 (GPR40) 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, there is a higher susceptibility to collagen-induced arthritis. The GPR40 agonist shows potential as a therapeutic agent. In the investigation of clinical patient samples, the study found that the expression of GPR40 in B lymphocytes is associated with the onset of the disease in RA patients.

　　Given the continuous development of therapies targeting GPR40, especially in the treatment of diabetes, these drugs may also be relevant to RA. Therefore, the evidence provided by this study can provide a reference for further research on the therapeutic potential of GPR40-targeted drugs in the management of RA.

　　DOI: https://doi.org/10.1016/j.celrep.2024.114858