IMMUNOPATHOLOGY IN THE EYES WITH EXPERIMENTAL UVEITIS

免疫活性细胞的特性和地形图定位以及 小鼠和啮齿类动物眼球停留细胞表面标志物的变化 对实验性自身免疫性葡萄膜视网膜炎(EAU)进行了分析 免疫组织化学研究和原位杂交。T淋巴细胞 大鼠EAU中以浸润性为主的细胞，但巨噬细胞和 T辅助者/诱导者是小鼠EAU的主要浸润细胞。T 淋巴细胞特异性是针对结合在一起的小段抗原。 细胞表面主要组织相容性复合体(MHC)分子，它们是 呈现在特殊的抗原提呈细胞的表面。这个 观察到眼部驻留细胞表达MHC-II类抗原 如视网膜色素上皮(RPE)、视网膜内皮细胞、角质形成细胞 啮齿动物的成纤维细胞和睫状体上皮细胞。MHC类的表达 Ii抗原立即被限制在眼部驻留细胞。 以局灶性病变为特征的小鼠EAU中的炎症部位 和慢性性。浸润性细胞亚群及其表达 眼部驻留细胞上II类抗原的比例可以通过各种不同的方式改变 免疫调节剂。 实验性内毒素诱导葡萄膜炎(EIU)是一种 人类的前葡萄膜炎。这种炎症的机制仍然是 不清楚，尽管磷脂酶A2(PLA2)的激活可能在 这种疾病的起源和传播。阿司匹林的药效研究 一种新的合成肽和一种PLA2抑制剂，抗氧化剂，显示 对大鼠EIU的抑制作用。血管的特殊结构 前葡萄膜与黏附分子(如细胞间)的作用 黏附分子和内皮细胞白细胞黏附分子)及其 在EIU中还检测了配体(淋巴细胞功能相关抗原)。 和Eau模特。

The identity and topographic localization of immunocompetent cells and the alteration of surface markers on ocular resident cells in mice and rodents with experimental autoimmune uveoretinitis (EAU) were analyzed by immunohistochemical studies and in situ hybridization. T lymphocytes were the predominantly infiltrating cells in rat EAU, yet both macrophages and T helpers/inducers were the predominant infiltrating cells in mouse EAU. T lymphocyte specificity is directed to small fragments of antigen bound to cell surface major histocompability complex (MHC) molecules, which are presented on the surface of specialized antigen-presenting cells. The expression of MHC class II antigens was observed on ocular resident cells such as retinal pigment epithelium (RPE), retinal endothelium, keratocytes, fibroblasts, and ciliary epithelium in rodents. The expression of MHC class II antigens is confined to ocular resident cells immediately at the inflammatory sites in mouse EAU, which was characterized by focal lesions and chronicity. Both the infiltrating cell subpopulation and the expression of class II antigens on ocular resident cells can be altered by various immunomodulating agents. Experimental endotoxin-induced uveitis (EIU) is a model for anterior uveitis in humans. The mechanism of this inflammation is still unclear, although activation of phospholipase A2 (PLA2) may play a role in the initiation and propagation of this disease. Study of the effect of a novel synthetic peptide and a PLA2 inhibitor, antiflammin, showed inhibition of EIU in rats. The particular vascular structure of the anterior uvea and the role of adhesion molecules (such as intercellular adhesion molecule and endothelial leukocyte adhesion molecule) and their ligand, (lymphocyte function-associated antigen) were also examined in EIU and EAU models.