Fig. 2

NF-κB activation in fibroblast-like synoviocytes regulate inflammatory responses in RA. Fibroblast-like synoviocytes play an important role in RA pathogenesis. NF-κB activation in FLS regulates different cell signaling processes, including decreasing FLS apoptosis by increasing the expression of anti-apoptotic genes and the inhibition of P53 and Fas as apoptosis regulatory molecules. NF-κB activation can also affect FLS proliferation and lead to FLS hyperplasia in RA synovium. Apart from this, RA-FLSs produce some growth factors which result in hyperplasia, inflammatory mediators such as inflammatory cytokines that maintain chronic inflammation in synovium, and different adhesion molecules which help further FLS migration to inflamed sites and increase their invasive characteristics. RA (Rheumatoid arthritis), NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), FLS (Fibroblast-like synoviocyte), Fas (CD95)