Schalken J J, Winkens H J, van Vugt A H, Bovée-Geurts P H, de Grip W J, Broekhuyse R M
Institute of Ophthalmology, University of Nijmegen, The Netherlands.
Exp Eye Res. 1988 Jul;47(1):135-45. doi: 10.1016/0014-4835(88)90030-9.
We have studied the clinicopathological features of experimental autoimmune uveoretinitis (EAU) induced in Lewis rats by injection of different doses of rhodopsin and its illuminated form opsin. Rhodopsin consistently appears to be more pathogenic than opsin. Injected in Freund's complete adjuvant and pertussis adjuvant 50 micrograms of rhodopsin induces a frequency of severe EAU similar to 250 micrograms of opsin. Intensity, frequency and location of ocular inflammation are markedly dose dependent. At high dose (100-250 micrograms), rhodopsin induces severe bilateral uveoretinitis in all animals, which starts with acute inflammation of the anterior eye segment at day 10-12 followed by chorioretinitis (predominantly retinitis) which results in complete elimination of the photoreceptor cells. At low dose (20 micrograms), rhodopsin induces mild transient inflammation in 60% of the animals, mainly consisting of mild posterior retinitis which starts at day 20 and leads to a typical multiple focal destruction of the photoreceptor cells. Intermediate doses cause an intermediate type of disease. Omission of pertussis adjuvant lowers the frequency of severe disease at low doses of rhodopsin, delays its onset and changes its features. The last characteristic has been observed in particular at intermediate doses (50-100 micrograms). In these cases, EAU usually starts by cell infiltration of the vitreous, while the anterior segment is only mildly affected. Without pertussis adjuvant the pathogenicity of opsin is low. Even in both adjuvants severe EAU can only be evoked by a high dose of opsin. Although there exists a marked difference in uveitogenicity between rhodopsin and opsin, the immunogenicity is similar and seems not to be correlated with their pathogenicity.
我们研究了通过注射不同剂量的视紫红质及其光照形式视蛋白在Lewis大鼠中诱导的实验性自身免疫性葡萄膜视网膜炎（EAU）的临床病理特征。视紫红质似乎始终比视蛋白更具致病性。在弗氏完全佐剂和百日咳佐剂中注射50微克视紫红质所诱导的严重EAU频率与250微克视蛋白相似。眼部炎症的强度、频率和部位明显依赖于剂量。高剂量（100 - 250微克）时，视紫红质在所有动物中诱导严重的双侧葡萄膜视网膜炎，在第10 - 12天从前段急性炎症开始，随后是脉络膜视网膜炎（主要是视网膜炎），导致光感受器细胞完全消失。低剂量（20微克）时，视紫红质在60%的动物中诱导轻度短暂炎症，主要由第20天开始的轻度后段视网膜炎组成，导致光感受器细胞典型的多发性局灶性破坏。中等剂量引起中间类型的疾病。省略百日咳佐剂会降低低剂量视紫红质时严重疾病的频率，延迟其发作并改变其特征。最后一个特征尤其在中等剂量（50 - 100微克）时观察到。在这些情况下，EAU通常从玻璃体的细胞浸润开始，而前段仅受到轻度影响。没有百日咳佐剂时，视蛋白的致病性较低。即使在两种佐剂中，高剂量视蛋白也只能诱发严重的EAU。尽管视紫红质和视蛋白在致葡萄膜炎性方面存在明显差异，但免疫原性相似，且似乎与其致病性无关。
