Broekhuyse R M, Kuhlmann E D, Winkens H J
Institute of Ophthalmology, University of Nijmegen, The Netherlands.
Exp Eye Res. 1992 Dec;55(6):819-29. doi: 10.1016/0014-4835(92)90008-g.
Purified retinal pigment epithelial cells of bovine eyes have been fractionated by a series of buffer and detergent extractions. The electropherogram of the buffer-insoluble, Triton X-100-soluble fraction (RPE-TS) exhibits a major polypeptide band of M(r) 65 kDa and a variety of minor components. Electrophoretically purified 65 kDa-band protein (PEP-65) is immunologically unrelated to the known uveitogenic photoreceptor proteins, to other neural retina proteins, and to PEP-X, the RPE-melanin-bound uveitogenic antigen. An immunocytochemical study of eye tissues suggests that it is exclusively located in the RPE. Immunization of Lewis rats with PEP-65 or affinity-purified RPE-TS induces a new type of ocular disease: experimental autoimmune posterior uveitis accompanied by epitheloid cell accumulations (monocytes) adjacent to the RPE (EAPU). The disease starts 9 days after immunization, provided that pertussis toxin is used as co-adjuvant. The first clinical signs are transient flare and cells in the anterior chamber. Choroiditis develops, and epitheloid cells accumulate focally along one or both sides of the Bruch's membrane-RPE layer. Such foci resemble, in some respects, Dálen-Fuchs nodules which occur in human sympathetic ophthalmia. Areas of inflammation are frequently localized in the chorioretinal periphery adjacent to the pars plana. Vitreous cell infiltration is the most prominent clinical feature of EAPU. During at least 2 months, extending chorioretinal areas containing epitheloid cell collections remain while the adjacent photoreceptor cells sometimes disappear without being invaded by these cells. Retinal vasculitis is seldomly observed and pinealitis is absent. EAPU has the latter feature in common with PEP-X-induced experimental autoimmune anterior uveitis (EAAU). The two diseases differ from the various photoreceptor antigen-induced forms of EAU where pinealitis and inflammation of the neural retina are prominent features. However, just as in EAU and EAAU, EAPU can be adoptively transferred, and is inhibited by cyclosporin treatment suggesting T-cell dependency.
通过一系列缓冲液和去污剂抽提对牛眼纯化的视网膜色素上皮细胞进行了分级分离。缓冲液不溶性、Triton X-100可溶性部分（RPE-TS）的电泳图谱显示出一条主要的分子量为65 kDa的多肽带以及多种次要成分。经电泳纯化的65 kDa条带蛋白（PEP-65）在免疫上与已知的致葡萄膜炎光感受器蛋白、其他神经视网膜蛋白以及与RPE-黑色素结合的致葡萄膜炎抗原PEP-X无关。对眼组织的免疫细胞化学研究表明，它仅位于视网膜色素上皮。用PEP-65或亲和纯化的RPE-TS免疫Lewis大鼠会诱发一种新型眼病：实验性自身免疫性后葡萄膜炎，伴有视网膜色素上皮（EAPU）附近的上皮样细胞聚集（单核细胞）。如果使用百日咳毒素作为共佐剂，疾病在免疫后9天开始。最初的临床症状是前房短暂的闪光和细胞。脉络膜炎发展，上皮样细胞沿布鲁赫膜-视网膜色素上皮层的一侧或两侧局部聚集。这些病灶在某些方面类似于人类交感性眼炎中出现的Dálen-Fuchs结节。炎症区域经常位于与睫状体平坦部相邻的脉络膜视网膜周边。玻璃体细胞浸润是EAPU最突出的临床特征。在至少2个月的时间里，含有上皮样细胞聚集的脉络膜视网膜区域不断扩大，而相邻的光感受器细胞有时会消失，且未被这些细胞侵袭。很少观察到视网膜血管炎，也没有松果体炎。EAPU与PEP-X诱导的实验性自身免疫性前葡萄膜炎（EAAU）有后一个共同特征。这两种疾病与各种光感受器抗原诱导的葡萄膜炎形式不同，在后者中，松果体炎和神经视网膜炎症是突出特征。然而，正如在葡萄膜炎（EAU）和实验性自身免疫性前葡萄膜炎（EAAU）中一样，EAPU可以被过继转移，并且环孢素治疗可抑制其发展，提示其依赖T细胞。
