Background: B lymphocyte-induced maturation protein 1 (Blimp1) is a risk allele for rheumatoid arthritis (RA), but its functional mechanism in RA remains to be further explored.Methods: Flow cytometry was performed to detect CD4 + T cell differentiation. ELISA was used to measure inflammatory factor secretion. Lentivirus mediated Blimp1 overexpression vector (LV-Blimp1) or short hairpin RNA (sh-Blimp1) were used to infect CD4 + T cells stimulated by anti-CD28 and anti-CD3 mAbs. RA fibroblast-like synoviocytes (FLSs) were co-cultured with CD4 + T cells or T cell conditioned medium (CD4CM), and cell proliferation, invasion, and expression of adhesion molecules and cytokines in FLSs were evaluated. Mice were injected intradermally with type II collagen to establish a collagen-induced arthritis (CIA) mouse model, and the severity of CIA was evaluated with H&E and Safranin-O staining. Results: Blimp1 knockdown increased pro-inflammatory factor secretion, but downregulated IL-10 concentration in activated CD4 + T cells. Blimp1 overexpression promoted regulatory T cells (Treg) CD4 + T cell differentiation and hindered T helper 1 (Th1) and T helper 17 (Th17) CD4 + T cell differentiation. Blimp1 overexpression suppressed the expression of pro-inflammatory factors and adhesion molecules in CD4 + T cells by upregulating IL-10. Moreover, Blimp1 overexpression impeded the enhanced effect of CD4 + T cells/CD4CM on cell adhesion, inflammation, proliferation, invasion and RhoA and Rac1 activities in FLSs by upregulating IL-10. Additionally, administration with LV-Blimp1 alleviated the severity of CIA. Conclusion: Blimp1 restrained CD4 + T cells-induced activation of FLSs by promoting the secretion of IL-10 in CD4 + T cells via the Rho signaling pathway.
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