Several studies have proposed a T-cell-mediated autoimmune reaction to antigenic protein from the uvea–retina as the pathogenic mechanism for the development of SO.^{[20,21,24,38]} Wong et al reported enhanced transformation of peripheral lymphocytes from patients with SO exposed to uveal–retinal extracts in tissue culture, suggesting that these patients have lymphocytes that are sensitized to components of uveal–retinal antigen.^[39] Various ocular antigens such as uveal melanin, uveal melanocytes, RPE, and retinal S-antigen have been implicated in the pathogenesis of SO in the past. In the animal model of uveitis, Rao et al showed that guinea pigs injected with retinal S-antigen developed an ocular inflammatory reaction similar to that of SO, including granulomatous panuveitis and focal collections of inflammatory cells at the level of RPE similar to Dalen–Fuchs nodules.^[40]Furthermore, experimental observations noted that intraocular injection with retinal S-antigen produced a …