Vernal keratoconjunctivitis (VKC) is a severe type of allergic conjunctival disease characterized by the presence both of various corneal epithelial and stromal lesions as well as of conjunctival proliferative changes such as giant papillae of the upper tarsal conjunctiva and limbal lesions. These clinical findings as well as various pathophysiological characteristics of VKC are distinct from those of other types of ocular allergy and allergic diseases of other organs. The outer eye possesses specific allergological characteristics, one of which is communication between the cornea and conjunctiva through a thin layer of tear fluid. Fibroblasts of the cornea and the conjunctiva are activated by proinflammatory and T helper 2 (Th2) cell-derived cytokines. Corneal fibroblasts enhance ocular allergic reactions as a result of their activation-induced expression both of chemokines such as eotaxin and TARC as well as of adhesion molecules such as ICAM-1 and VCAM-1, all of which together promote the activation and infiltration of eosinophils and Th2 lymphocytes. In contrast, corneal epithelial cells suppress such reactions by physically separating corneal fibroblasts from bioactive substances in tear fluid. Exaggerated proliferation of and deposition of extracellular matrix by conjunctival fibroblasts likely exacerbate conjunctival inflammation. Restoration of an intact corneal epithelium and inhibition of the activities of corneal and conjunctival fibroblasts may provide a basis for the development of new treatments for severe ocular allergic diseases such as VKC.