Infection with the parasitic nematode Onchocerca volvulus can lead to severe visual impairment and blindness. In an effort to characterize the molecular basis for the inflammatory response in the cornea, we have developed a murine model for O. volvulus-mediated keratitis in which parasite antigens are injected into the corneal stroma of sensitized mice. This model reproduces the two main clinical features of human disease, corneal opacification and neovascularization. Histological analysis of corneas from these mice reveals a biphasic recruitment of neutrophils and eosinophils to the central cornea, along with a small, but persistent number of CD3+ cells. In this review, we present evidence that production of antigen-specific T cell and antibody responses are essential for development of O. volvulus keratitis, and we propose a sequence of molecular and cellular events that lead to migration of inflammatory cells to the cornea and to loss of corneal clarity.