Figure 1.

Role of neutrophil in the pathogenesis of RA. Proinflammatory cytokines in the joint can influence the migration of neutrophils. Neutrophils are activated by immune complexes and inflammatory cytokines (TNF-α, IL-6, IL-8, and IL-17a) within the synovial fluid, frequently causing enhanced NET formation in RA. In turn, NETs are served as a source of citrullinated autoantigens, further triggering the production of ACPA. Meanwhile, neutrophils undergo delayed apoptosis in an inflammatory milieu (GM-CSF, IL-9, IL-15, IFN-γ, and TNF-α) leading to persistent inflammation and joint damage in RA. ^∗Controversial.