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1 From the Laboratory of Immunology and the 2 Laboratory of Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland.
PURPOSE. Experimental autoimmune uveoretinitis (EAU) is a T-cell–mediated disease induced by immunization with interphotoreceptor retinoid binding protein (IRBP). Major uveitogenic sites have been identified for mice of the H-2r and H-2k haplotypes but not for the H-2b haplotype. The present communication describes the characterization of an epitope contained in residues 1 to 20 of human IRBP that induces EAU in H-2b mice.
METHODS. H-2b (C57BL/6, 129/J) and H-2r (B10.RIII) mice were immunized with peptide 1-20 or with whole (bovine) IRBP. EAU (histopathology) and immunologic responses (delayed-type hypersensitivity [DTH], lymphocyte proliferation, and cytokine production) were assessed after 21 days.
RESULTS. C57BL/6 mice, 129/J and (129/JxC57BL/6)F1 mice, immunized with 200 to
300 µg of peptide, developed DTH and EAU with scores comparable to
those induced by 100 µg IRBP. Their lymphocytes proliferated to the
peptide and produced interferon-
(but not interleukin-4) and
transferred EAU to syngeneic recipients. Lymphocytes of IRBP-immunized
mice also responded to the peptide. Peptide 1-20–immunized B10.RIII
mice failed to develop either disease or immunologic responses.
CONCLUSIONS. Human IRBP peptide 1-20 contains a major epitope for the H-2b haplotype, which is apparently not presented by the H-2r haplotype.
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