白细胞介素22在类风湿关节炎中的作用机制研究OA

Rheumatoid arthritis(RA)is a chronic autoimmune disease pathologically characterized by symmetrical synovitis of small joints,and its pathogenesis has not yet been fully elucidated.Recent studies have found that interleukin-22(IL-22)plays dual roles at different stages of RA and under different cytokine microenvironments,mainly exerting pro-inflammatory and bone destruction-promoting effects,or protective effects under specific conditions.This article systematically reviews the mechanisms of IL-22 in the course of RA,summarizes recent findings on its activation of downstream signaling networks affecting fibroblast-like synoviocytes(FLS)and osteoclasts(OC),and analyzes the molecular basis and clinical translational potential of IL-22 as a key regulator of inflammation and bone destruction,thereby providing a theoretical basis for novel targeted therapies for RA.IL-22 is an inflammatory cytokine that activates the Janus kinase(JAK)/signal transducer and activator of transcription(STAT),mitogen-activated protein kinase(MAPK),nuclear factor(NF)-κB,and phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)signaling pathways by binding to the IL-22 receptor.It plays dual pro-inflammatory and anti-inflammatory roles in cell proliferation,apoptosis and immune responses.By regulating the generation,differentiation and immune responses of FLS and OC,IL-22 participates in the occurrence and development of RA,leading to synovial inflammation,pannus formation and bone destruction in the joints of patients with RA.