In this study we have investigated the involvement of SOCS proteins in regulating ocular inflammatory diseases of infectious or autoimmune etiology. We recently showed that SOCS3 deletion in T Lymphocytes suppresses the development of chronic ocular inflammation by up-regulating CTLA-4 and inducing the expansion of regulatory T cells. In ongoing studies we are using transgenic rats that over-express SOCS1 in the retina and mice with targeted deletion of SOCS1 in the retina to further elucidate the role of SOCS1 and SOCS3 in ocular diseases. Thus far, our data have revealed that topical SOCS1 antagonists can be useful in suppressing ocular HSV-1 infection and mitigating herpetic stromal keratitis. On the other hand, topical administration of a SOCS1 mimetic peptide inhibits ocular inflammation and mitigates ocular pathology during mouse uveitis
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