Experimental autoimmune uveoretinitis (EAU) is a T-cell mediated autoimmune disease that serves as a model of human intraocular inflammatory disease (uveitis). It is initiated in susceptible animals by immunization with retinal antigens such as interphotoreceptor retinoid-binding protein (IRBP) and S-Antigen (SAg) or by adoptive transfer of ocular Ag-specific uveitogenic T cells. We and others have demonstrated that T lymphocytes expressing T-cell receptor (TCR) of the Vbeta8 family are implicated in the pathogenesis of EAU. In fiscal year 1995, we sought to determine whether T cells of the gamma delta lineage also play a role in EAU and in human uveitic conditions. We analyzed the TCR Vgamma repertoire in the retinas of Lewis rats with and without EAU as well as the repertoire of several SAg- or IRBP-specific T-cell lines. We found a correlation between detection of Vgamma2+ T cells and EAU pathogenesis; TCR Vgamma2 transcripts were detected in all four pathogenic lines and in the retinas of Lewis rats with EAU but not in the two nonpathogenic lines nor in the retinas of naive rats. With regard to human uveitic conditions, our analysis was restriced to patients with ocular sarcoidosis. Analysis of the gammadelta TCR repertoire revealed a relative abundance of gammadelta+ T cells in the lacrimal gland of patients with ocular sarcoidosis. Taken together, our results suggest a possible involvement of these cells in the pathogenesis or control of inflammatory tissue damage during sarcoidosis and EAU.
