The role and mechanism of IL‑35 in myasthenia gravis (Review)

Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by impaired neuromuscular junction transmission, leading to fluctuating muscle weakness and fatigue. This condition is driven primarily by autoantibodies targeting the acetylcholine receptor at the neuromuscular junction. These antibodies are predominantly generated through a T‑cell‑dependent pathway, initiating immunomodulatory responses via complement activation. Cytokines and inflammatory mediators also play pivotal roles in the pathogenesis of MG. Recently, increasing attention has been given to the involvement of cytokines in autoimmune diseases. Interleukin‑35 (IL‑35), an immunoregulatory cytokine, is critical in various inflammatory and autoimmune conditions. It modulates immune responses by promoting Treg proliferation, enhancing their immunosuppressive functions, inhibiting Th17 cell differentiation, and reducing proinflammatory cytokine levels. IL‑35 is thus pivotal in the onset and progression of MG. The present review outlines the key functions of IL‑35 in MG pathogenesis and the impact of IL‑35 on the treatment and prognosis of myasthenia gravis, explores its therapeutic potential, and assesses its prognostic value, offering insights into its mechanisms and implications for treatment.