Shek P N, Waltenbaugh C, Coons A H
J Exp Med. 1978 Apr 1;147(4):1228-35. doi: 10.1084/jem.147.4.1228.
The simultaneous administration of colchicine (CC) with a T-independent antigen, e.g. 2,4,6-trinitrophenyl-keyhold limpet hemocyanin-Sepharose, to intact animals effectively enhanced their hapten-specific plaque-forming cell (PFC) response. However, in congenitally athymic nude mice in which T-cell regulation was absent, CC was ineffective in producing enhancement. These observations suggest that the target cell acted upon by CC is most likely thymus-derived. Furthermore, the injection of CC with the co-polymer of L-glutamic acid50-L-tyrosine50 (GT) abolished GT-specific suppression of the PFC response to GT-methylated bovine serum albumin. Spleen cells from CC-treated and GT-primed hosts could no longer transfer suppressive activity to normal recipients. These results provide evidence that CC is capable of inactivating or eliminating suppressor cells or their precursors. Thus, CC-induced enhancement of the antibody response may be explained, at least in part, by its antimitotic, and hence lethal effect on dividing suppressor T cells.
将秋水仙碱(CC)与非胸腺依赖性抗原(如2,4,6-三硝基苯基-钥孔血蓝蛋白-琼脂糖)同时给予完整动物,可有效增强其半抗原特异性空斑形成细胞(PFC)反应。然而,在先天性无胸腺裸鼠中,由于缺乏T细胞调节,CC在产生增强作用方面无效。这些观察结果表明,CC作用的靶细胞很可能是胸腺来源的。此外,将CC与L-谷氨酸50-L-酪氨酸50(GT)的共聚物一起注射,消除了GT对GT-甲基化牛血清白蛋白的PFC反应的特异性抑制。来自CC处理和GT致敏宿主的脾细胞不再能够将抑制活性传递给正常受体。这些结果提供了证据,证明CC能够使抑制细胞或其前体失活或消除。因此,CC诱导的抗体反应增强至少部分可以通过其抗有丝分裂作用,进而对分裂的抑制性T细胞产生致死作用来解释。