Dumonde D C, Kasp-Grochowska E, Banga J P, Sanders M D, Graham E, Stanford M A, Faure J P, De Kozak Y, Van Tuyen V
Trans Ophthalmol Soc U K (1962). 1985;104 ( Pt 3):232-8.
This paper summarises the principal immunopathological mechanisms which may underlie ocular inflammation and draws attention to how autoimmune reactions may be regulated by idiotypic networks of the immune system. The study of autoimmunity in inflammatory eye disease is illustrated by our current investigations of retinal vasculitis in man and of experimental autoimmune uveoretinitis in rodents where three lines of evidence indicate that immune complex formation may be a compensatory host response to the development of antiretinal autoimmunity. In discussing immunological implications of these results we suggest that retinal inflammation in antiretinal autoimmunity is limited by a protective anti-idiotypic antibody response and that retinal disease arises when this compensatory response is improperly balanced. The clinical implications of this reasoning include the identification of patients at risk of relapse of ocular disease and the development of therapeutic methods for restoring an imbalanced anti-idiotypic autoimmune response towards normality.
本文总结了可能是眼部炎症基础的主要免疫病理机制，并提请注意自身免疫反应如何由免疫系统的独特型网络调节。人类视网膜血管炎和啮齿动物实验性自身免疫性葡萄膜视网膜炎的当前研究说明了炎症性眼病自身免疫的研究，其中三条证据表明免疫复合物形成可能是宿主对抗视网膜自身免疫发展的一种代偿反应。在讨论这些结果的免疫学意义时，我们认为抗视网膜自身免疫中的视网膜炎症受到保护性抗独特型抗体反应的限制，当这种代偿反应失衡时就会出现视网膜疾病。这种推理的临床意义包括识别有眼部疾病复发风险的患者，以及开发将失衡的抗独特型自身免疫反应恢复正常的治疗方法。
