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Cellular immune response to Ia induction by intraocular gamma-interferon
1Department of Ophthalmology, Washington University School of Medicine, St. Louis, Mo.
BALB/c mice and Lewis rats were injected intraocularly with recombinant gamma-interferon (IFN-gamma). The distribution of Ia antigens and cellular infiltrates was studied over a 21-day time course. In mice, Ia antigens were induced on cells in the corneal stroma, corneal endothelium, iris, ciliary body, retinal pigment epithelium and cells in the retina. No detectable cellular infiltrate accompanied class II major histocompatibility (MHC) antigen induction in mice. In rats, cells in all of the intraocular tissues mentioned above were induced to express Ia antigens. However, in distinct contrast to mice, the induction of Ia antigens on intraocular structures in rats was accompanied by intense cellular inflammation composed predominantly of polymorphonuclear cells. These findings demonstrate that aberrant Ia expression on intraocular tissues by IFN-gamma is not sufficient to elicit a cellular autoimmune response in mice. The observed species-related differences in cellular immune response to class II MHC antigen induction on intraocular tissues parallels the susceptibility of mice and rats to experimental autoimmune uveitis.
BALB/c mice and Lewis rats were injected intraocularly with recombinant gamma-interferon (IFN-gamma). The distribution of Ia antigens and cellular infiltrates was studied over a 21-day time course. In mice, Ia antigens were induced on cells in the corneal stroma, corneal endothelium, iris, ciliary body, retinal pigment epithelium and cells in the retina. No detectable cellular infiltrate accompanied class II major histocompatibility (MHC) antigen induction in mice. In rats, cells in all of the intraocular tissues mentioned above were induced to express Ia antigens. However, in distinct contrast to mice, the induction of Ia antigens on intraocular structures in rats was accompanied by intense cellular inflammation composed predominantly of polymorphonuclear cells. These findings demonstrate that aberrant Ia expression on intraocular tissues by IFN-gamma is not sufficient to elicit a cellular autoimmune response in mice. The observed species-related differences in cellular immune response to class II MHC antigen induction on intraocular tissues parallels the susceptibility of mice and rats to experimental autoimmune uveitis.