Purpose of review: Osteoarthritis has been considered a degenerative disease. However, recent evidence supports involvement of immunologic mechanisms in this pathophysiology: for example, inflammation of synovial tissue is observed in osteoarthritis. In osteoarthritis, the proinflammatory cytokine interleukin-1, which is produced by activated synoviocytes and mononuclear cells and has catabolic effects on chondrocytes, is one of the most involved. The immune reaction would require driving antigens. This review describes autoantigens in osteoarthritis and discusses their roles in triggering and/or perpetuating synovitis and joint cartilage destruction in osteoarthritis.
Recent findings: Several autoantigens/autoantibodies have been reported in osteoarthritis, such as the cartilage intermediate layer protein. Furthermore, recent comprehensive proteomic surveillance has revealed that comparable numbers of autoantigens were detected in osteoarthritis and rheumatoid arthritis, and that some of them were recognized predominantly in osteoarthritis rather than in rheumatoid arthritis. In addition, it was revealed that the cartilage intermediate layer protein immunization of mice developed calcification of tendons, thus indicating that autoimmunity modulates functions of target molecules.
Summary: Osteoarthritis-specific autoantigens may drive chronic synovitis and may thereby contribute to production of cytokines to upregulate proteases, which lead to chondrocyte and cartilage damage. In addition, autoimmunity may damage joint components by modulating functions of the target molecules.
Copyright 2004 Lippincott Williams & Wilkins