FasL autoantibodies in vasculitis are associated with the presence of anticorneal epithelial antibodies.

Eye complications are common in vasculitis, especially in Wegener’s granulomatosis (WG), where up to 50% of all cases have ophthalmic involvement. Eye involvement in the Churg-Strauss syndrome (CSS) has been reported but is rare. Corneal autoantigens have been documented in patients with WG and CSS; in particular, circulating autoantibodies to corneal specific keratin 3 (K3) are present in 60% of patients with WG. Most of these patients have peripheral ulcerative keratitis (PUK), but others have no detectable eye disease. Antibodies to a second corneal antigen, BCEA-B, are associated with CSS. The eye is an immune privileged organ characterised by a reduced or modified immune response which protects the eye from inflammation and autoimmunity. Fas, together with its ligand FasL, has an important role in maintaining ocular immune privilege. Fas+ lymphoid cells that enter the eye are killed by apoptosis when the Fas binds with FasL present on ocular structures. When the Fas/FasL system is defective in mice a direct inflammatory insult to the eye triggers an inflammatory response that overwhelms the eye and causes significant damage. 5 Anti-FasL autoantibodies have been found in patients with systemic lupus erythematosus (SLE) and may be involved in the immune abnormalities and pathogenesis of this condition. These autoantibodies appear to protect lymphocytes from apoptosis by binding to FasL, leaving it unable to bind to Fas. Autoantibodies to FasL may be present in patients with vasculitis. If present, these antibodies may compromise ocular immune privilege and contribute to eye complications and/or the production of antibodies to ocular antigens. Therefore the main aim of this study was to detect FasL antibodies in sera from patients with vasculitis with and without PUK.