IMMUNOPATHOLOGY IN THE EYES WITH EXPERIMENTAL AUTOIMMUNE UVEITIS

免疫活性细胞的身份和拓扑定位 和眼常驻细胞表面标志物的改变， 啮齿类动物实验性自身免疫性葡萄膜视网膜炎， 免疫或过继转移分析， 免疫组织化学研究。 淋巴细胞群在 发现炎症部位在治疗过程中发生了显著变化。 病程。 在早期阶段，辅助性T细胞/诱导物是 眼内的主要细胞。 T的相对增加- 在晚期观察到抑制/细胞毒性细胞。 主要组织相容性复合体II类抗原的表达 在眼驻留细胞如RPE，视网膜内皮， 角膜基质细胞、成纤维细胞和睫状体上皮 不同型号的EAU。 这种抗原表达可能起作用， 在EAU的发病中起一定作用。 既渗透， 可以调节II类抗原细胞亚群的改变 环孢素和地塞米松治疗。

Identity and topographic localization of immunocompetent cells and alteration of surface marker on ocular resident cells in rodents with experimental autoimmune uveoretinitis by active immunization or adoptive transfer were analyzed by immunohistochemical studies. The lymphocyte population at the inflammatory sites was found to change markedly during the course of disease. In the early stage, T-helper/inducers are the predominant cells in the eye. A relative increase of T- suppressor/cytotoxic cells in the late stage were observed. Expression of major histocompatibility complex class II antigens on ocular resident cells such as RPE, retinal endothelium, keratocytes, fibroblast and ciliary epithelium was observed in different models of EAU. This antigen expression may play a certain role in the pathogenesis of EAU. Both infiltrating and alteration of class II antigens cell subpopulation can be modulated by cyclosporine and dexamethosone treatment.