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The Journal of Immunology, 2001, 167: 919-925.
Copyright © 2001 by The American Association of Immunologists

A Dominant Role for Fc{gamma} Receptors in Antibody-Dependent Corneal Inflammation1

Laurie R. Hall, Eugenia Diaconu and Eric Pearlman2

Departments of Medicine and Ophthalmology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106

Although production of specific Ab is a critical element of host defense, the presence of Ab in tissues leads to formation of immune complexes, which can trigger a type III Arthus reaction. Our studies on a mouse model of river blindness showed that Ab production is essential for recruitment of neutrophils and eosinophils to the cornea and for development of corneal opacification. In the current study, we determined the relative contribution of complement and Fc{gamma}R interactions in triggering immune complex-mediated corneal disease. Fc{gamma}R-/- mice, C3-/- mice, and immunocompetent control (B6/129Sj) mice were immunized s.c. and injected intrastromally with Onchocerca volvulus Ags. Slit lamp examination showed that control mice, C3-/- mice, and control mice injected with cobra venom factor developed pronounced corneal opacification, whereas corneas of Fc{gamma}R-/- mice remained completely clear. Furthermore, recruitment of neutrophils and eosinophils to the corneal stroma was significantly impaired in Fc{gamma}R-/- mice, but not in C3-/- mice or cobra venom factor-treated mice. We therefore conclude that Fc{gamma}R-mediated cell activation, rather than complement activation, is the dominant pathway of immune complex disease in the cornea. These findings demonstrate a novel role for Fc{gamma}R interactions in mediating ocular inflammation.




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