Fig. 3
From: Targeting pathogenic fibroblast-like synoviocyte subsets in rheumatoid arthritis
Targeting signaling pathways that drive pathogenic FLS differentiation might be a potential strategy for the treatment of RA. FLSs exhibit high phenotypic plasticity, and different cytokines or cells can stimulate the differentiation of different FLS subsets. Targeting NOTCH3 signaling at FLSs might affect CD90 expression in FLSs. IFN-γ-mediated stimulation of JAK-STAT1 signaling might also block HLA-DR expression in CD90+FLSs, which has proinflammatory effects during RA pathogenesis