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FasL antibodies may compromise ocular immunity and so allow antibodies to corneal antigens to form, rather than directly causing eye disease, suggests a study of 34 patients with vasculitis.
The study was prompted by the knowledge that various corneal autoantigens have been found in patients with Wegener’s granulomatosis and Churg-Strauss syndrome—most, but not all of whom, have peripheral ulcerative keratitis.
The presence of autoantibodies to FasL, K3, and BCEA-B was sought in 18 patients with Wegener’s granulomatosis (WG) but no eye complications; seven with peripheral ulcerative keratitis (PUK); nine with Churg-Strauss syndrome (CSS); and in 14 people with no eye disease.
FasL antibodies were detected in two WG (11%) and two PUK patients. Significantly, BCEA-B antibodies were also found in all four of these patients, but in only four (12.5%) of the patients without FasL antibodies.
None of the patients positive for K3 antibodies carried antibodies to FasL, but one in four of those without FasL antibodies carried K3 antibodies. None of the patients with FasL antibodies had eye complications.
The authors conclude that it’s not clear whether the apparent link between FasL antibodies and antibodies to ocular antigens is causal or coincidental. But they suggest that antibodies to FasL may block FasL function in the eye and compromise its ability to withstand inflammation and autoimmune disease.
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