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C.–H. Yang, F.–A. Lin, C.–P. Lin, C.–M. Yang, M.–S. Chen; Expression of Lymphotactin and Its Receptor in Lewis Rat With Experimental Autoimmune Anterior Uveitis . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4542.
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© ARVO (1962-2015); The Authors (2016-present)
To demonstrate the expression of C chemokine, lymphotactin, and its receptor, XCR, in the iris/ciliary body and popliteal lymph node and thus establish their roles in experimental autoimmune anterior uveitis, an animal model of human acute anterior uveitis.
Uveitis was induced in Lewis rats by injection of melanin associated antigen into the peritoneum and footpad. The rats were sacrificed on days 0, 5, 10, 14, 21 and 27 of post–immunization. At defined times; lymphotactin and its receptor XCR mRNA expression in the iris/ciliary body and popliteal lymph node were measured by using a semiquantitative polymerase chain reaction method. Lymphotactin in aqueous humor and serum were determined by enzyme linked immunosorbent assay after immunization and after NF–ΚB inhibitor, pyrrolidine dithiocarbamate (PDTC; 200 mg/kg/day) treatment in a separate experiment. The cellular sources of lymphotactin were determined by immunhistochemical staining and flow cytometry.
Lymphotactin receptor, XCR, mRNA was found to be upregulated in the iris/ciliary body five days after immunization, preceding clinical disease onset. Lymphotactin mRNA exhibited peak levels at day 14, coincident with disease onset. Lymphotactin in serum showed a preceding expression profile, which were causative subsequently cloudy gel–like aqueous humor and clinical disease onset. PDTC (200 mg/kg) markedly inhibited the expression of lymphotactin in the aqueous humor and serum. Immunohistochemical staining revealed that lymphotactin was expressed on infiltrated inflammatory cells of iris/ciliary body. Flow cytometry analysis revealed that there was increasing number of CD8 + cytotoxic T cells with positive lymphotactin staining with the severity degree of inflammation.
The sequential expression of lymphotactin receptor, XCR, may direct distinct lymphotactin expressing lymphocytes subsets to inflammatory sites. This increase of lymphotactin expressing lymphocytes subsets to inflammatory sites may account for the fact that the number of infiltrating lymphocytes was relatively high in the peak stage. Lymphotactin could attract more inflammatory cells to the iris/ciliary body and its expression is modulated, at least in part, through the NF–ΚB signaling pathway.
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