Vasodilation, chemotaxis, and principal mechanisms that cause inflammation through IgG ICs.

A study of 430 RA patients revealed a strong correlation between C3a levels and disease activity, particularly in those without RF or ACPA. This suggests that seropositive RA patients have complement depletion.

C3a has been shown to promote the expression of proinflammatory cytokines (e.g., TNF-α and IL-1β) in monocytes and synovial fibroblasts, suggesting that it plays a direct role in amplifying local joint inflammation.

As an opsonin to ICs and its complement receptor.

Promote phagocytosis of complement-activated cells.

Discovered in RA patients’ degenerating cartilage but lacking in healthy cartilage, suggesting the activation of the classical pathway of the complement system.

As an opsonin to ICs and its complement receptor.

Significant reduction in seropositive RA patients, indicating complement consumption due to IC development.

According to a 2012 genetic study, C4B gene deficiency was twice as prevalent in RA patients compared to controls, particularly in those who had seropositive status and shared epitope.

Vasodilation, chemotaxis, and principal mechanisms that cause inflammation through IgG ICs. Activation of mast cells and macrophages enhances the expression of activating FcγRs and suppresses the expression of inhibitory FcγRIIB.

C5a regulates osteoclast formation and bone resorption, linking it to RA joint destruction. The C5a-C5aR1 axis is being focused on to investigate bone-related pathologies in RA.

C5a was shown to stimulate migration and activation of synovial neutrophils, contributing to pannus formation and chronic synovitis in RA patients.