Marak G E, Font R L, Alepa F P
Mod Probl Ophthalmol. 1976;16:75-9.
Experimental lens-induced granulomatous endophthalmitis is an experimental autoimmune disease that is histopathologically identical to the human disease known as phacoanaphylactic endophthalmitis or lens-induced uveitis. The capacity to develop experimental disease after lens injury can be passively transferred to virgin animals with hyperimmune serum. Fluorescein-labeled anti-IgG and anti-C'3 antisera bind to the lenses of appropriately sensitized animals after lens injury but not to the injured lenses of unsensitized control animals. Cobra Venom factor which inhibits C'3 prevents the development of lens-induced granulomatous uveitis in appropriately sensitized animals. Hypersensitized animals develop a massive Arthus-like reaction. On the basis of these observations we feel that experimental lens-induced granulomatous endophthalmitis is an immune complex disease. Because the experimental disease is histopathologically identical to human lens-induced uveitis or phacoanaphylactic endophthalmitis we believe an immune complex mechanism of immunopathogenesis is important in phacoanaphylactic endophthalmitis.
实验性晶状体诱导性肉芽肿性眼内炎是一种实验性自身免疫性疾病,其组织病理学特征与人类的晶状体过敏性眼内炎或晶状体诱导性葡萄膜炎相同。晶状体损伤后发生实验性疾病的能力可通过超免疫血清被动转移至未接触过抗原的动物。荧光素标记的抗IgG和抗C'3抗血清在晶状体损伤后可与致敏动物的晶状体结合,但不与未致敏对照动物的损伤晶状体结合。抑制C'3的眼镜蛇毒因子可防止致敏动物发生晶状体诱导性肉芽肿性葡萄膜炎。超敏动物会出现大量类似Arthus反应。基于这些观察结果,我们认为实验性晶状体诱导性肉芽肿性眼内炎是一种免疫复合物疾病。由于实验性疾病在组织病理学上与人类晶状体诱导性葡萄膜炎或晶状体过敏性眼内炎相同,我们认为免疫复合物免疫发病机制在晶状体过敏性眼内炎中很重要。