[Corneal ulcerative lesions in type-I immediate hypersensitivity].

The vernal keratoconjunctivitis (KCV) is included within the category of the hypersensitiveness diseases, the immunopathological mechanism which causes the disease being represented by a type-I hypersensibility reaction. The mechanism which determines the appearance of the corneal lesions isn't entirely cleared up, but there are however some pathogenic links which have been already deciphered. The type I hypersensibility reaction is taking place within two stages: stage I the stage of the sensitizing contact and stage II the stage of the unleashing contact. During the first stage, the Langerhans cells take over and process the allergen, exhibiting on their surface only the antigenic part. The Langerhans cells interact with the T helper native cells (Tho), cells from which there will result the predominantly differentiated Th2 subtype. The Thz cells will activate, by means of the interleukines, the B cells (which produce the IgE), the mast cells and the eosinophilic cells. During the second stage, the allergen is coming into contact with the IgE specific antibodies, which are fastened on the mast cells membrane, generating the opening of their granules. The result of this evolution is represented by the unleash of vasoactive mediators, own enzymes, chemical mediators (among which there is also the eosinophilic chemotactic factor ECFA). The latter contributes to the infiltration of the epithelial and of the subepithelial tissue with eosinophilic cells. The major basic protein (PBM), one of the proteins released from the eosinophilic cells' big granules, plays a major pathogenic role in the production of the corneal ulcer, by means of its direct cytotoxic effect and also by means of inhibiting the migration of the epithelial corneal cells. The role of the mast cells and also the role of the neutrophile cells within the framework of the pathogenesis of the ulcer is disputable, because some specific enzymes tryptase, respectively elastase--have been found within the debris of the corneal ulcer. The allergic keratoconjunctivitis (KCA) represents the ocular manifestation of the systemic hypersensitiveness. In the beginning the immunopathogenic mechanism which causes the lesions is represented by a type-I hypersensibility reaction, but during its evolution, the characteristic histopathological changes (chronic granulomas, perivascularitis, subendothelial fibrosis) are suggesting a complex immunoregulatory disfunction.