Wetzig R, Hooks J J, Percopo C M, Nussenblatt R, Chan C C, Detrick B
Laboratory of Immunology, National Eye Institute, Bethesda, MD 20892.
Curr Eye Res. 1988 Aug;7(8):809-18. doi: 10.3109/02713688809033212.
An experimental model of inflammatory eye disease, experimental autoimmune uveitis (EAU), was established by injecting rats in the footpad with S-antigen in complete Freund's adjuvant. This model system was used to evaluate the role of major histocompatibility complex (MHC) class II antigens (Ia) in the pathogenesis of this T cell mediated disease. One day prior to S-antigen priming, rats were injected with either anti-Ia antibodies or with mouse ascites. Clinical and histopathological analysis of eyes from rats treated with anti-Ia antibody showed less ocular inflammation as well as a delay in onset of EAU when compared to controls (p = 0.01). Furthermore, immunocytochemical evaluation demonstrated that tissue obtained from animals receiving anti-Ia therapy also expressed less Ia antigen, as well as a diminution in the number of infiltrating macrophages and lymphocytes. These data show that anti-Ia treatment significantly modifies the course of EAU in the rat. In addition, this study suggests that MHC class II antigen expression may be involved in the initiation and continuation of immune responses that results in ocular inflammatory diseases.
通过在大鼠足垫注射完全弗氏佐剂中的 S 抗原，建立了炎性眼病实验模型——实验性自身免疫性葡萄膜炎（EAU）。该模型系统用于评估主要组织相容性复合体（MHC）II 类抗原（Ia）在这种 T 细胞介导疾病发病机制中的作用。在 S 抗原致敏前一天，给大鼠注射抗 Ia 抗体或小鼠腹水。与对照组相比，用抗 Ia 抗体治疗的大鼠眼睛的临床和组织病理学分析显示眼部炎症较轻，且 EAU 发病延迟（p = 0.01）。此外，免疫细胞化学评估表明，接受抗 Ia 治疗的动物所获得的组织中 Ia 抗原表达也较少，浸润的巨噬细胞和淋巴细胞数量也减少。这些数据表明抗 Ia 治疗显著改变了大鼠 EAU 的病程。此外，本研究表明 MHC II 类抗原表达可能参与导致眼部炎性疾病的免疫反应的启动和持续。
