Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent joint inflammation. Cytokine play a significant role in the pathogenesis of RA, contributing to synovial inflammation and joint destruction.

 In particular, pro-inflammatory Cytokine such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17) have been implicated in promoting the inflammatory response in RA. Targeting these cytokines and their signalling pathways has revolutionized the treatment landscape for RA.

Biologic therapies, such as TNF inhibitors and IL-6 receptor antagonists, have shown remarkable efficacy in reducing disease activity and improving clinical outcomes in RA patients. The identification of specific Cytokine targets has opened up new avenues for developing targeted therapeutic interventions tailored to the underlying immunopathology of RA.

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