Greenwood J
Department of Clinical Science, Institute of Ophthalmology, London, UK.
Curr Eye Res. 1992;11 Suppl:25-32. doi: 10.3109/02713689208999508.
The blood-retinal barrier (BRB) is believed to play an important part in the pathogenesis of experimental autoimmune uveoretinitis (EAU). Central to the disease process is the recruitment of inflammatory cells from the circulation, a mechanism that is controlled in part by the BRB. As the disease progresses the BRB becomes disrupted first to small and then to large molecular weight tracers. In these two respects EAU shares many similarities with experimental autoimmune encephalomyelitis (EAE) in which there is dysfunction of the blood-brain barrier (BBB). In EAU, however, the differential roles played by the two barrier sites that comprise the BRB are not clear although some evidence would suggest that it is the retinal endothelium that is initially involved. BRB breakdown in EAU has been found to occur concomitantly with lymphocyte infiltration by mechanisms that remain to be elucidated.
血视网膜屏障（BRB）被认为在实验性自身免疫性葡萄膜视网膜炎（EAU）的发病机制中起重要作用。疾病过程的核心是炎症细胞从循环系统的募集，这一机制部分受BRB控制。随着疾病进展，BRB首先对小分子然后对大分子示踪剂的屏障功能遭到破坏。在这两个方面，EAU与血脑屏障（BBB）功能障碍的实验性自身免疫性脑脊髓炎（EAE）有许多相似之处。然而，在EAU中，构成BRB的两个屏障部位所起的不同作用尚不清楚，尽管一些证据表明最初涉及的是视网膜内皮。已发现EAU中的BRB破坏与淋巴细胞浸润同时发生，但其机制仍有待阐明。
