Broekhuyse R M, Stekhoven J H, Arends M
Institute of Ophthalmology, University of Nijmegen, The Netherlands.
Exp Eye Res. 1991 Aug;53(2):141-9. doi: 10.1016/0014-4835(91)90067-o.
Experimental autoimmune retinitis induced by immunization with rhodopsin was investigated in the Lewis rat using transmission electron microscopy and light microscopy. The first signs of retinitis consisted of scattered infiltrations of lymphocytes and other mononuclear cells, predominantly in the inner nuclear layer and outer plexiform layer. Occasionally, some macrophages were detected in the photoreceptor cell layer. Eyes exhibiting a clinically moderate or severe inflammation contained areas of normal retina coexistent with mildly to severely inflamed foci. The central retina was more frequently affected than the peripheral area. In moderately inflamed foci, macrophages infiltrated the photoreceptor cell layer, damaging and eliminating its structures. Inflammatory cells penetrated the photoreceptor outer segment layer which remained unaltered so far in spite of a high serum anti-(rhod)opsin antibody titer. In stages of severe inflammation, massive infiltrations of macrophages and polymorphonuclear cells destroyed the photoreceptor cells focally, leaving the retinal pigment epithelium virtually unaffected. Adjacent to these foci the pigment epithelial cells sometimes exhibited increased numbers of phagosomes and swelling. The locations of the cell infiltrations and lesions in progressive stages of development suggest that the rod outer segments are the target for the autoimmune damage. The described patterns of inflammation were compared with those of previous studies using other animal species and inciting antigens. Especially in rhodopsin-induced retinitis, the blood-retina barrier at the level of the Bruch's membrane/pigment epithelium appears to be highly resistant to cytotoxic cells. The present observations are in agreement with the concept that the cellular immune response plays a major role in the pathogenesis of (rhod)opsin-induced retinitis.
利用透射电子显微镜和光学显微镜，在Lewis大鼠中研究了用视紫红质免疫诱导的实验性自身免疫性视网膜炎。视网膜炎的最初迹象包括淋巴细胞和其他单核细胞的散在浸润，主要位于内核层和外丛状层。偶尔，在光感受器细胞层中检测到一些巨噬细胞。表现出临床中度或重度炎症的眼睛含有与轻度至重度炎症灶共存的正常视网膜区域。视网膜中央比周边区域更常受到影响。在中度炎症灶中，巨噬细胞浸润光感受器细胞层，破坏并消除其结构。炎症细胞穿透光感受器外节层，尽管血清抗（视）紫红质抗体滴度很高，但该层至今仍未改变。在严重炎症阶段，巨噬细胞和多形核细胞的大量浸润局部破坏了光感受器细胞，而视网膜色素上皮几乎未受影响。在这些病灶附近，色素上皮细胞有时吞噬体数量增加且肿胀。细胞浸润和病变在疾病进展阶段的位置表明，视杆外节是自身免疫损伤的靶标。将所描述的炎症模式与先前使用其他动物物种和激发抗原的研究进行了比较。特别是在视紫红质诱导的视网膜炎中，脉络膜/色素上皮水平的血视网膜屏障似乎对细胞毒性细胞具有高度抗性。目前的观察结果与细胞免疫反应在（视）紫红质诱导的视网膜炎发病机制中起主要作用的概念一致。
