Immune mechanisms in autoimmune ocular disease.

Abstract

Aberrant expression of Class II MHC antigens (Ia) by non-immune cells is considered to be an important mechanism in the pathogenesis of autoimmune disease processes including those affecting the eye. It is suggested that circulating autoreactive T-cells are directed to their target organ as a result of aberrant expression of Ia antigens by the vascular endothelium of that organ. This hypothesis was tested in this study using two different models of severe ocular inflammation, induced by either S-antigen or bovine serum albumin (BSA). The retinal vascular endothelium becomes Ia + in S-antigen induced inflammation but not in inflammation induced by BSA. The accumulation in the eye of a T-cell line, ThS, specific for an ocular antigen (S-antigen), was compared in the two types of ocular inflammation and compared to that of another T-cell line, ThP, specific for a non-ocular antigen (PPD). In S-antigen induced inflammation, there was much greater accumulation of ThS than ThP whereas in BSA induced inflammation, both T-cell lines accumulated to the same extent but more than in uninflamed eyes. These results suggest that when the retinal vascular endothelium expresses Ia antigens during an inflammatory process, autoreactive T-cells will be specifically retained in the eye as a result of this and perpetuate the autoimmune destructive process.