Vernal conjunctivitis (VC), a bilateral conjunctival disease, is a cause of significant eye disease in many individuals each year. The seasonal incidence, the presence of eosinophils in tear secretions and the response to topical or systemic steroid therapy suggest an immune hypersensitivity reaction to an environmental agent. The proposed study is designed to elucidate the pathogenesis of tissue injury and the etiology of this disease. Initial studies have demonstrated specific IgE antibodies to pollen allergens in the tear secretions of 54.5% of patients with VC. This suggests that other immune mechanisms, although not mutually exclusive with an IgE-mediated hypersensitivity, may also be important in the pathogenesis of VC. External ocular secretions (tear fluid) of VC patients will be studied for the presence of class specific antibody activity (IgG, IgM, IgA) to pollen antigens by the ELISA system. The presence of immune complexes/complement components and specific antibodies may suggest a complement mediated hypersensitivity mechanism. Direct evidence for an immune mechanism in the pathogenesis of VC will be sought by examining tear fluids for the biologically active mediators of inflammation. Since eosinophils in the conjunctival secretions are a prominent feature in VC, tear secretions will be studied for the presence of a factor(s) which influences the migration of eosinophils. An IgE-mediated, a complement-derived or T-cell mediated immune mechanism can result in the generation of leukokinetic or leukotactic factors for eosinophils. The characterization and identification of these factors in tears together with the other studies outlined above would define the immune hypersensitivity mechanism(s) which play an important role in the pathogenesis of VC.
