de Bara R, Kusuda M, Caspers-Velu L, Sanui H, Chan C C, Kuwabara T, Nussenblatt R B, Gery I
Laboratory of Immunology, National Eye Institute, Bethesda, Maryland.
Invest Ophthalmol Vis Sci. 1989 Oct;30(10):2165-73.
Treatment of rat eyes with cryopexy enhanced the development of experimental autoimmune uveitis (EAU) in these eyes. The enhancement of EAU by cryopexy was particularly pronounced when the disease was induced by active immunization in rats of a low responder strain (Wistar Furth), or by adoptive transfer with lymphocytes sensitized against S-antigen. The disease enhancement was expressed by earlier onset of clinical symptoms and by more severe inflammatory changes. Histological examination of cryopexy-treated eyes showed focal necrosis and inflammation, confined to the affected sites. Immunohistochemical analysis of the inflammatory infiltration revealed it consists mainly of macrophages and T-lymphocytes of the helper and suppressor subsets. In addition, increased expression of class II antigens was observed in affected areas, on both inflammatory and resident ocular cells. Using electron microscopy and Evans blue angiography we could show breakdown of the blood-retinal barrier at the treated sites. Histological examination of eyes with EAU following cryopexy showed localization of the early inflammation at the injured site. The data are interpreted to suggest that the enhanced EAU in cryopexy-treated eyes is mainly due to the breakdown of the blood-retinal barrier, the accumulation of lymphoid cells and the increased expression of class II antigens, which facilitates antigen presentation.
对大鼠眼睛进行冷冻治疗会增强这些眼睛中实验性自身免疫性葡萄膜炎(EAU)的发展。当在低反应性品系(Wistar Furth)的大鼠中通过主动免疫诱导疾病,或通过用针对S抗原致敏的淋巴细胞进行过继转移诱导疾病时,冷冻治疗对EAU的增强作用尤为明显。疾病增强表现为临床症状更早出现以及炎症变化更严重。对接受冷冻治疗的眼睛进行组织学检查显示,局部坏死和炎症局限于受影响部位。对炎症浸润进行免疫组织化学分析发现,其主要由辅助性和抑制性亚群的巨噬细胞和T淋巴细胞组成。此外,在受影响区域,炎症细胞和眼部驻留细胞上均观察到II类抗原表达增加。使用电子显微镜和伊文思蓝血管造影,我们可以显示治疗部位的血视网膜屏障遭到破坏。对冷冻治疗后患有EAU的眼睛进行组织学检查显示,早期炎症定位于损伤部位。这些数据被解释为表明,冷冻治疗的眼睛中EAU增强主要是由于血视网膜屏障的破坏、淋巴细胞的积聚以及II类抗原表达增加,这有利于抗原呈递。