The interferon (IFN) proteins can modify a variety of biological activities and are considered one of the body's regulatory proteins. Numerous studies now indicate that the IFN's are potent immunoregulators. During the past year we have been studying the ways in which IFN proteins interact with cells of the immune system and how this interaction may modify immune responses and immunologically related disorders. Using immunocytochemical analysis we have developed a sensitive method of identifying lymphokines, IFN-gamma and IL2, at the site of tissue damage. We have identified these lymphokines in inflammatory eye diseases. The presence of these lymphokines is associated with a lymphocyte infiltrate predominantly of a T-cell origin and with the expression of MHC class II antigens on both the infiltrating cells and in the retinal pigment epithelial (rpe) cells. Experimentally we have shown that this direct intravitreal inoculation of recombinant rat IFN-gamma results in the expression of MHC Class II antigen (Ia) in a variety of ocular cells. This is the first demonstration of lymphokines, IFN-gamma and IL2 at the site of a localized autoimmune disease. These observations may indicate that IFN-gamma induced MHC class II antigen expression may serve as a local amplification system in autoimmune and inflammatory eye disease. A better understanding of the role of lymphokines in the mechanisms involved in the development of autoimmunity and inflammation may be beneficial in the treatment of these diseases.
