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Blimp1 suppressed CD4+ T cells‐induced activation of fibroblast‐like synoviocytes by upregulating IL‐10 via the rho pathway
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. 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. 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. 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.
Blimp1 suppressed CD4+ T cells‐induced activation of fibroblast‐like synoviocytes by upregulating IL‐10 via the rho pathway
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. 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. 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. 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.
Blimp1 suppressed CD4+ T cells‐induced activation of fibroblast‐like synoviocytes by upregulating IL‐10 via the rho pathway
Meng, Qingliang (author) / Wen, Zhike (author) / Meng, Wanting (author) / Bian, Hua (author) / Gu, Huimin (author) / Zuo, Ruiting (author) / Zhan, Junping (author) / Wang, Huilian (author) / Miao, Xiyun (author) / Fan, Wei (author)
Environmental Toxicology ; 38 ; 146-158
2023-01-01
13 pages
Article (Journal)
Electronic Resource
English