IMMUNOPATHOLOGY IN THE EYES WITH EXPERIMENTAL UVEITIS

免疫活性细胞的特性和地形图定位 小鼠眼内停留细胞表面标志物的变化及意义 实验性自身免疫性葡萄膜视网膜炎(EAU)的啮齿动物 通过免疫组织化学研究和原位杂交进行分析。 T淋巴细胞是大鼠EAU中主要的浸润性细胞， 然而，巨噬细胞和T辅助细胞/诱导物都是主要的 小鼠EAU内有细胞浸润性。炎性细胞的迁移 由黏附分子引导从血管进入靶点 可在血管内皮细胞和其他驻留细胞上表达 眼睛。T淋巴细胞特异性是针对小片段的 细胞表面主要组织相容性复合体(MHC)抗原 分子，它们呈现在特化的表面 抗原提呈细胞。MHC-II类抗原的表达 在视网膜色素等眼部驻留细胞上观察到 上皮(RPE)、视网膜血管内皮细胞、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的表达 II类抗原立即被限制在眼部驻留细胞 小鼠EAU的炎性部位，以局灶性病变为特征 病变和慢性化。浸润性细胞亚群和 眼部驻留细胞上II类抗原的表达可以是 被各种免疫调节剂改变。 实验性内毒素诱导性葡萄膜炎(EIU)是一种前葡萄膜炎模型 人类患葡萄膜炎。这种炎症的机制仍然是 尚不清楚，尽管磷脂酶A2(PLA2)的激活可能起到 在这种疾病的发生和传播中起着重要作用。特别之处 前葡萄膜的血管结构及其粘连作用 分子(如细胞间黏附分子和内皮细胞 白细胞黏附分子)及其配体(淋巴细胞 功能相关抗原)也在EIU和EAU中进行了检测 模特们。PLA2(氯丙嗪、安非他明等)的抑制作用和 黏附分子可以消除EIU。

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 predominantly infiltrating cells in mouse EAU. The migration of inflammatory cells from vessels into target sites is directed by adhesion molecules that can be expressed on vascular endothelium and other resident cells in the eye. T-lymphocyte specificity is directed to small fragments of antigen bound to cell surface major histocompatibility 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 vascular 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 is 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. 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) also were examined in EIU and EAU models. Inhibition of PLA2 (chlorpromazine, antiflammin, etc.) and adhesion molecules can abrogate EIU.