Abstract

Anti-fibronectin autoantibodies (AFA) have been detected in the serum and synovial fluid of patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and systemic vasculitis; they predominantly recognize the native form of the antigen. In SLE, these antibodies are directed mainly against the 30 kDa collagen-binding domain of the fibronectin molecule and they correlate with disease activity and musculoskeletal manifestations. However, since AFA are not specific to any particular autoimmune disease, their diagnostic value is low. The pathogenic potential of anti-fibronectin antibodies has been investigated by blocking fibronectin interactions with other extracellular matrix components and cells. It was shown that as a target antigen, fibronectin is involved in immune complex diseases and cartilage destruction. Anti-fibronectin autoantibodies are detected by enzyme-linked immunosorbent assay (ELISA) in roughly 29–78% of patients with SLE, 14–40% of those with RA, and 7% of patients with Behçet's disease. Anti-fibronectin IgM antibodies were present in 8% of patients with SLE. Anti-fibronectin antibodies are also present in a number of bacterial and viral infections, such as those caused by Mycoplasma pneumoniae and Legionella pneumophila and in endocarditis, syphilis, and leprosy. The diagnostic value of anti-fibronectin antibodies is low. Since AFA are not specific for any autoimmune disease, their routine determination cannot be recommended. There are no data available on the prognostic value of anti-fibronectin antibodies. Further studies are required to clarify the significance of AFA for the pathogenesis of autoimmune diseases.

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