Our study suggested that one of the mechanisms that a few T cells initiate autoimmune uveitis is that IRBP-specific T cells interact with parenchymal cells such as residential DCs [49], microglia [50], astrocytes [51], and Müller cells [52], resulting in the subsequent production of HMGB1 by those cells, mediated by Fas/FasL, an early event in the pathogenesis of intraocular inflammation. Here, FAS is linked to autoimmune uveitis.