Hara Y, Caspi R R, Wiggert B, Chan C C, Streilein J W
Department of Microbiology and Immunology, University of Miami School of Medicine, FL 33101.
Curr Eye Res. 1992;11 Suppl:97-100. doi: 10.3109/02713689208999517.
Experimental Autoimmune Uveitis (EAU) was induced by immunization with bovine interphotoreceptor retinoid binding protein (IRBP) in B10.A mice. The experiments were performed to evaluate whether Anterior Chamber Associated Immune Deviation (ACAID) can be induced by IRBP when injected intracamerally. The results indicate that anterior chamber (AC) injection of IRBP impaired the development of IRBP-specific delayed hypersensitivity and prevented the expression of EAU following immunization with IRBP-CFA. Adoptive transfer of spleen cells obtained from mice that received IRBP into AC suppressed EAU, whether administered prior to or after the uveitogenic regimen. Most important, IRBP-specific suppressor cells from AC-IRBP treated mice when injected into IRBP-EAU mice suppressed and eliminated already established intraocular inflammation. IRBP-specific, ACAID-inducing suppressor T cells act on the efferent limb of the immune response, and represent ideal modalities for treating already established EAU.
通过用牛视网膜色素上皮间维生素A结合蛋白(IRBP)免疫B10.A小鼠诱导实验性自身免疫性葡萄膜炎(EAU)。进行这些实验以评估当眼内注射IRBP时是否能诱导前房相关免疫偏离(ACAID)。结果表明,眼内注射IRBP会损害IRBP特异性迟发型超敏反应的发展,并在用IRBP-完全弗氏佐剂免疫后预防EAU的表达。将从接受IRBP眼内注射的小鼠获得的脾细胞进行过继转移可抑制EAU,无论在致葡萄膜炎方案之前还是之后给药。最重要的是,将来自眼内注射IRBP处理小鼠的IRBP特异性抑制细胞注射到IRBP-EAU小鼠中可抑制并消除已确立的眼内炎症。IRBP特异性、诱导ACAID的抑制性T细胞作用于免疫反应的传出支,是治疗已确立的EAU的理想方式。