INTRAOCULAR CLASS II ANTIGEN EXPRESSION IN ENDOTOXIN-INDUCED UVEITIS

内毒素是一种来源于革兰氏阴性菌细胞壁的多糖 阴性细菌。 当注射到脚垫或眼睛， 它会在眼睛内引起炎症反应。 的 这种炎症的机制尚不清楚。 但由于 人类的几种前葡萄膜炎似乎与 革兰氏阴性菌暴露，这被认为是相对的 用于人的前葡萄膜炎例如赖特综合征的模型。 在这项研究中，大鼠接受E.大肠杆菌内毒素的表达 II类抗原在眼内进行了研究， 免疫组织化学技术。 我们观察到 睫状体和虹膜上II类抗原的表达 预防炎症细胞流入眼睛， 进入眼睛的炎症细胞主要是 中性粒细胞和一些单核细胞。 没有T细胞存在于 炎性浸润。 炎性细胞浸润 可以被消炎痛或秋水仙碱抑制，但事实确实如此 不改变虹膜或纤毛II类抗原的表达 身体表明这个表达式不仅仅是一个结果 炎症浸润，但也可能与 内毒素诱导葡萄膜炎表达的机制。 皮质类固醇能够抑制细胞内 炎症浸润和II类抗原的表达。 免疫组化显示非淋巴样细胞上的II类抗原表达， 眼睛在抗原呈递中可能是重要的， 由于以下物质的相互作用而在细胞上发出表型变化的信号 内毒素与细胞膜接触。 结果进行了比较 在被动和主动免疫中表达II类抗原 眼内Arthus。

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. 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 inflammatory 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 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. The findings were compared with the expression of class II antigen in passive and active intraocular Arthus.