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Editor,—We read with interest the Newsdesk piece in the March 2000 issue of theBJO,1 commenting on recent studies indicating a conceptual shift in the understanding of the molecular basis of differential susceptibility to organ specific autoimmune diseases. However, we were disappointed that the Newsdesk piece was restricted to studies of the animal model of multiple sclerosis and not that of uveitis. In a paper published in 19972 we demonstrated that ocular specific antigens (S-antigen (arrestin) and interphotoreceptor retinoid binding protein (IRBP)), which are targets for pathogenic autoimmune processes, are expressed in the thymus of certain animals. Furthermore, we found that animals which express S-antigen or IRBP in their thymus are resistant to experimental autoimmune uveoretinitis induced by the corresponding molecule, whereas the absence of thymic expression correlates with susceptibility.
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