INTRAOCULAR CLASS II ANTIGEN EXPRESSION IN ENDOTOXIN-INDUCED UVEITIS

内毒素是一种来源于革兰氏阴性杆菌细胞壁的多糖， 细菌 当注射到老鼠的足垫或眼睛里时， 引起眼睛内的炎症反应。 内毒素注射 脚垫不会导致其他器官炎症，但会产生 双侧葡萄膜炎主要集中在睫状体和虹膜。 的 这种炎症的机制尚不清楚。 然而，由于几个 人类前葡萄膜炎的类型似乎与革兰氏阴性 细菌暴露，这被认为是前葡萄膜炎的相对模型 比如赖特综合征 在这项研究中，大鼠接受E.杆菌 内毒素和II类抗原的表达进行了研究， 眼用免疫组织化学技术。 我们观察到， 睫状体和虹膜上的II类抗原的存在预示着 炎症细胞进入眼睛， 眼睛主要是中性粒细胞和一些单核细胞。 没有T细胞 存在于炎性浸润中。 第二类的表达 眼内抗原仅限于虹膜和睫状体， 这种炎症发作并不涉及视网膜色素 上皮或视网膜血管。 炎性细胞浸润 被吲哚美辛或秋水仙碱抑制，但这并没有改变 虹膜或睫状体表达II类抗原，表明 这种表达不仅仅是炎症浸润的结果 但可能与基因表达的机制密切相关， 内毒素诱导的葡萄膜炎。 皮质类固醇能够抑制 细胞炎性浸润和II类抗原表达 抗原 非淋巴样细胞上II类抗原的表达， 眼睛在抗原呈递中可能是重要的 由于内毒素与细胞的相互作用， 细胞膜

Endotoxin is a polysaccharide derived from the cell wall of gram negative bacteria. When injected into the footpad or the eye of a rat it will induce an inflammatory reaction within the eye. Endotoxin injection in the footpad does not lead to inflammation in other organs but does produce bilateral uveitis primarily centered at the ciliary body and iris. The mechanism of this inflammation is still unclear. However, since several types of anterior uveitis in humans appear to be linked to gram negative bacteria exposure, this is considered a relative model for anterior uveitis in humans such as Reiter's syndrome. In this study rats received E. coli endotoxin and the expression of class II antigens was studied within the eye using immunohistochemical techniques. We observed that the expression of class II antigens on the ciliary body and iris preceeded the influx of inflammtory cells into the eye and that the inflammatory cells that entered the eye were primarily neutrophils with some monocytes. No T-cells were present in the inflammatory infiltrate. The expression of class II antigens withing the eye was restricted to the iris and ciliary body during this inflammatory episode and did not involve the retinal pigment epithelium or retinal vessels. The inflammatory cellular infiltrate could be inhibited by indomethacin or colchicine, however this did not alter the expression of class II antigens by the iris or ciliary body indicating that this expression is not simply a consequence of the inflammatory infiltrate but may be intimately involved with the mechanism of the expression of endotoxin induced uveitis. Corticosteroids were capable of suppressing both the cellular inflammatory infiltrate and the expression of class II antigens. The expression of class II antigens on nonlymphoid cells within the eye may be important in antigen presentation or may simply signal a phenotypic change on the cells due to the interaction of endotoxin with the cell membranes.