Fig. 1

NF-κB activation perpetuates chronic inflammation by targeting genes involved in inflammation during RA development. NF-κB activation in innate and adaptive immune cells can be responsible for inflammatory responses and perpetuating chronic inflammation in RA synovium. NF-κB activation in T cells results in T cell signaling, activation, and differentiation in inflammatory T cells which produce inflammatory cytokines and maintain inflammation in rheumatoid synovium. Impaired Treg function in RA patients can be related to Foxp3 downregulation and is due to the overexpression of inflammatory cytokines such as TNF-α in the RA microenvironment. Moreover, B cell proliferation and auto-antibody production is deeply connected with activated NF-κB members. In terms of innate immune regulation, deregulated NF-κB activation in dendritic cells can cause the induction of cytokines which promote inflammatory T cell differentiation. These repeating cycles can exacerbate disease severity. NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), RA (Rheumatoid arthritis), Foxp3 (Forkhead box P3), TNF-α (Tumor necrosis factor alpha)