de Kozak Y, Mirshahi M, Boucheix C, Faure J P
Unité de Recherche d'Ophtalmologie, INSERM U 86-CNRS, Institut Biomédical des Cordeliers, Paris, France.
Reg Immunol. 1989 Sep-Oct;2(5):311-20.
Preimmunization of rnu/+ rats with the mouse monoclonal antibody S2D2 against retinal S-antigen (S-Ag) leads to an anti-idiotypic (anti-Id) response and to protection against experimental autoimmune uveoretinitis (EAU) provoked by a subsequent challenge with S-Ag in complete Freund's adjuvant (CFA). Suppression of EAU can be passively transferred using lymph node and/or spleen cells from donors with active anti-Id immunity to naive rnu/+ recipients, prior to immunization with bovine S-Ag in CFA. In contrast, passive administration of IgG from S2D2-immunized rats did not produce suppression. High levels of anti-Id S2D2 antibodies were found: (1) in rats presenting an inhibited EAU after sensitization with S2D2 or after passive transfer of anti-S2D2 cells prior to the S-Ag immunization; and (2) in rats with a severe EAU after transfer of anti-S2D2 IgG associated with anti-S2D2 cells prior to the S-Ag challenge. No effect on the anti-S-Ag antibody level could be detected. These experiments suggest that EAU, a mostly T cell-dependent disease, can be down regulated by anti-Id lymphoid cells.
用抗视网膜S抗原（S-Ag）的小鼠单克隆抗体S2D2对rnu/+大鼠进行预免疫，会引发抗独特型（抗Id）反应，并对随后在完全弗氏佐剂（CFA）中用S-Ag激发的实验性自身免疫性葡萄膜视网膜炎（EAU）产生保护作用。在CFA中用牛S-Ag免疫之前，可将具有活性抗Id免疫的供体的淋巴结和/或脾细胞被动转移给未免疫的rnu/+受体，从而被动转移EAU的抑制作用。相比之下，被动给予S2D2免疫大鼠的IgG并未产生抑制作用。发现高水平的抗Id S2D2抗体：（1）在用S2D2致敏后或在S-Ag免疫前被动转移抗S2D2细胞后出现EAU抑制的大鼠中；（2）在S-Ag激发前转移与抗S2D2细胞相关的抗S2D2 IgG后出现严重EAU的大鼠中。未检测到对抗S-Ag抗体水平的影响。这些实验表明，EAU这种主要由T细胞介导的疾病，可被抗Id淋巴细胞下调。
