Eisenfeld A J, Bunt-Milam A H, Saari J C
Exp Eye Res. 1987 Mar;44(3):425-38. doi: 10.1016/s0014-4835(87)80176-8.
Interphotoreceptor retinoid-binding protein (IRBP) is a glycoprotein found in the interphotoreceptor matrix between the neurosensory retina and the retinal pigment epithelium and is thought to shuttle retinol among cells that border the interphotoreceptor space. Immunization of rabbits with bovine IRBP caused subsequent photoreceptor degeneration, as documented by light- and electron microscopy. Beginning on post-injection day 18, scattered regions had photoreceptor outer segments that were disorganized and shortened or absent. Macrophages were found between the retinal pigment epithelium and neurosensory retina and within choroidal interstitium and blood vessels. Labeling of these cells with a marker specific for monocytic macrophages (RAM11) and absence of labeling with a marker for retinal pigment epithelium (rabbit anti-bovine cellular retinaldehyde-binding protein) suggest that these macrophages were hematogenous in origin. Staining of retinas with fluorescein isothiocyanate (FITC)-conjugated sheep anti-rabbit IgG revealed leakage of rabbit IgG into the interphotoreceptor matrix on and after day 18 in experimental animals but not in controls, suggesting breakdown of the outer blood-retinal barrier. Indirect immunofluorescence with anti-glial fibrillary acidic protein revealed labeling of Müller cells in experimental retinas on and after day 18, but not in control or shorter survival experimental retinas. There were foci of increased cellularity in the choroid on days 18, 26 and 39. From days 26 through 67, the retinal pathology became more widespread. Varying degrees of outer-segment degeneration were present in all parts of the retina and in many areas there was total loss of outer segments and loss of some photoreceptor-cell bodies. The inner retina appeared unaffected in all experimental and control retinas. These results demonstrate that injection of rabbits with bovine IRBP causes retinal photoreceptor degeneration as anti-IRBP titers increase and breakdown of the outer blood-retinal barrier ensues. Further studies will be required to elucidate factor(s) that control accessibility of the neurosensory retina to circulating antibodies against IRBP and other intrinsic retinal proteins.
光感受器间类视黄醇结合蛋白（IRBP）是一种存在于神经感觉视网膜和视网膜色素上皮之间的光感受器间基质中的糖蛋白，被认为在与光感受器间空间相邻的细胞之间穿梭视黄醇。用牛IRBP免疫兔子会导致随后的光感受器退化，这已通过光学显微镜和电子显微镜记录。从注射后第18天开始，散在区域的光感受器外段出现紊乱、缩短或缺失。在视网膜色素上皮和神经感觉视网膜之间以及脉络膜间质和血管内发现了巨噬细胞。用单核巨噬细胞特异性标记物（RAM11）标记这些细胞，而用视网膜色素上皮标记物（兔抗牛细胞视黄醛结合蛋白）未标记，表明这些巨噬细胞起源于血源性。用异硫氰酸荧光素（FITC）偶联的羊抗兔IgG对视网膜进行染色，结果显示，在实验动物中，第18天及之后兔IgG渗漏到光感受器间基质中，而对照组则未出现这种情况，这表明外血视网膜屏障遭到破坏。用抗胶质纤维酸性蛋白进行间接免疫荧光显示，在第18天及之后的实验性视网膜中，米勒细胞有标记，但在对照组或存活时间较短的实验性视网膜中则没有。在第18、26和39天，脉络膜出现细胞增多灶。从第26天到67天，视网膜病变变得更加广泛。视网膜各部位均出现不同程度的外段退化，许多区域外段完全丧失，部分光感受器细胞体也丧失。在所有实验性视网膜和对照视网膜中，内视网膜似乎未受影响。这些结果表明，给兔子注射牛IRBP会随着抗IRBP滴度的增加导致视网膜光感受器退化，并随之出现外血视网膜屏障的破坏。需要进一步研究以阐明控制神经感觉视网膜对循环抗IRBP抗体和其他视网膜固有蛋白的易感性的因素。
