Much of the above mostly in vitro work investigating basic cellular processes has obvious, but untested relevance for translational science. Preclinical physiologic, pharmacologic, and therapeutic studies rely on experimental models, and my initial interest in ocular inflammation and immune privilege was not diverted irrevocably by our studies in cell biology. Indeed, the issue of why inflammation in the eye was “blunted” has been my main interest since those early days of curiosity as to why blood in the vitreous failed to clear. I, therefore, began to ask questions about inflammation and immune privilege in the eye. To study this, I was fortunate that the model of experimental autoimmune uveoretinitis (EAU) had been developed recently, including the discovery of the major retinal autoantigen, retinal S antigen.
24 With reagents from WB Wacker (Proctor Lecturer in 1991), we set up the EAU model in the guinea pig and rat, and with Paul McMenamin, long-time friend and colleague, and now sponsor, we performed some definitive electron microscopy studies.
25–27 Later, we used R Caspi's (Freidenwald lecturer in 2011) model of EAU in the mouse,
28 and currently are using the chronic relapsing model in the C57/BL6 mouse.
29 This is an excellent model that closely mirrors the disease in humans, and has been the cornerstone of many basic immunologic studies revealing the mixed role of various types of T cells in the pathogenesis of this disease.
30,31