Age-associated B cells contribute to the pathogenesis of rheumatoid arthritis by inducing activation of fibroblast-like synoviocytes via TNF-α-mediated ERK1/2 and JAK-STAT1 pathways - Qin, Yi; Cai, Ming-Long; Jin, Hui-Zhi; Huang, Wei; Zhu, Chen; Bozec, Aline; Huang, Jingang; Chen, Zhu (Annals of the rheumatic diseases, 2022)
Keywords: Age; Animals; Antibodies; Arthritis, Experimental - pathology; Arthritis, Rheumatoid; Autoimmune diseases; B-Lymphocytes; Cells, Cultured; Chemotaxis; Collagen; Collagenase 3; Culture Media, Conditioned; Cytokines; Disease; Extracellular signal-regulated kinase; Fibroblasts; Fibroblasts - metabolism; Flow cytometry; Immunological memory; Inflammation; Interferon; Interferons; Interleukin 6; Interleukin-6 - metabolism; Interstitial collagenase; Janus kinase; Janus Kinases - metabolism; Joint diseases; Lupus; Lymphocytes B; MAP Kinase Signaling System; Matrix metalloproteinase; Matrix Metalloproteinase 1 - metabolism; Matrix Metalloproteinase 13 - metabolism; Matrix Metalloproteinase 3 - metabolism; Memory cells; Mice; Pathogenesis; Phenotypes; Phosphorylation; Rheumatoid arthritis; Signal transduction; Spleen; Stat1 protein; STAT1 Transcription Factor; Synovial fluid; Synovial Membrane - metabolism; Synoviocytes; Synoviocytes - metabolism; synovitis; Tumor Necrosis Factor-alpha - metabolism; Western blotting; China; B-Lymphocytes; arthritis, rheumatoid; fibroblasts; synovitis