IL-33: A promising therapeutic target for rheumatoid arthritis
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammatory disease including synovial proliferation and excessive pro-inflammatory cytokines production leading to cartilage and bone destruction. Several proinflammatory cytokines are considered critical in forming the inflammatory process of RA including IL-1, IL-6, IL-8, IL-15, and TNF-alpha. Approximately, 1% of the world's population is affected by this disease and is commonly associated with functional disability and reduced quality of life.
Cytokine-mediated immunity plays a crucial role in the pathogenesis of various autoimmune diseases including RA. Recently, IL-1 family member IL-33 was recognized to perform as an inflammatory cytokine, exerted profound effects in human RA and experimental inflammatory arthritis. Moreover, administration of IL-33 leads to the development of severe inflammatory arthritis, suggesting that IL-33 may be therapeutically relevant in RA and the targeting of IL-33 or the IL-33 receptor has been proposed as a potential therapeutic approach for autoimmune diseases such as RA.
Recent studies reported the correlation of IL-33 with rheumatic diseases and most of them found that IL-33 expression levels were consistent with disease activity and development. Furthermore, evidence has indicated that IL-33-related treatment may ameliorate the pathogenic conditions and attenuate disease progression of those rheumatic diseases. Therefore, elucidation of the roles of IL-33 in rheumatic diseases would be beneficial to understand the pathogenesis and therapy of these diseases. It is hoped that this information may aid the development of novel therapeutic strategies for RA.