Schalken J J, Winkens H J, Van Vugt A H, De Grip W J, Broekhuyse R M
Institute of Ophthalmology, University of Nijmegen, The Netherlands.
Br J Ophthalmol. 1989 Mar;73(3):168-72. doi: 10.1136/bjo.73.3.168.
We present the first evidence that purified rhodopsin can induce experimental autoimmune uveoretinitis (EAU) in monkeys. Injection of a highly purified lipid-free rhodopsin preparation provokes severe chorioretinitis with concomitant anterior uveitis. The onset of disease is earlier, its frequency is higher, and the inflammation is considerably more severe than in EAU induced under similar conditions by opsin. The first inflammatory cells are observed in the ciliary body and pars plana. Within a few days the inflammation extends into the anterior chamber, choroid, and retina. Retinitis predominates in the central area, while chorioretinitis is observed in the periphery, both accompanied by damage to and elimination of the photoreceptor cells. The monkeys develop high cellular and humoral immune responses against rhodopsin and opsin. The cellular response maximum just precedes the onset of EAU. This may indicate that cellular immunity has an important role in the pathogenesis of rhodopsin-induced EAU.
我们提供了首个证据，证明纯化的视紫红质可在猴子中诱发实验性自身免疫性葡萄膜视网膜炎（EAU）。注射高度纯化的无脂质视紫红质制剂会引发严重的脉络膜视网膜炎，并伴有前葡萄膜炎。与在类似条件下由视蛋白诱导的EAU相比，疾病的发作更早，频率更高，炎症也更严重得多。最早的炎症细胞出现在睫状体和平坦部。几天内，炎症蔓延至前房、脉络膜和视网膜。视网膜炎症在中央区域占主导，而脉络膜视网膜炎则出现在周边区域，两者均伴有光感受器细胞的损伤和清除。猴子针对视紫红质和视蛋白产生了高度的细胞免疫和体液免疫反应。细胞反应高峰恰好在EAU发作之前出现。这可能表明细胞免疫在视紫红质诱导的EAU发病机制中起重要作用。
