Clinical experiments in cellular immunity in eye disease.

Experiments with leukocyte migration inhibition (LMI) in various ocular disorders indicate sensitivity to cornea and lens most frequently, and to retina, choroid, and iris less often. The immunologist's dictum that sensitivity develops to "foreign" proteins is borne out since cornea and lens are relatively, if not completely, avascular after birth. Herpes virus infection of the cornea not only induces vascularity but exposes the lymphocyte to a cell not previously known to it and possibly transformed by viral DNA. The release of lymphokines such as lymphotoxin may increase pathology. Other mediators of cellular immunity (blastogenic, migration inhibitory, and leukotactic factor) may assist healing by "walling" the antigen in a granuloma as in tuberculosis. It is not known which mediator is of greater importance in viral keratitis, toxoplasmic chorioretinitis, and retinal detachment. Lens protein appears not to enter the circulation after cataract extraction. Severe inflammation adjacent to the lens may sensitize the lymphocyte to lens protein, lead to lymphotoxin secretion, and enhance lens damage. Other in vitro tests must be used to study cell-mediated immunity since LMI has shown that it is involved in many ophthalmologic conditions.