Kim Y T, Goidl E A, Samarut C, Weksler M E, Thorbecke G J, Siskind G W
J Exp Med. 1985 May 1;161(5):1237-42. doi: 10.1084/jem.161.5.1237.
After immunization with trinitrophenyl (TNP)-Ficoll, mice produced both anti-TNP antibodies and auto-anti-idiotype (auto-anti-Id) antibodies specific for the anti-TNP antibody. Older animals produced more auto-anti-Id than did young animals. When mice were exposed to a normally lethal dose of irradiation while their bone marrow (BM) was partially shielded, they survived and slowly (6 wk) regained immune function, as indicated by the number of nucleated cells in their spleen and the in vitro primary plaque-forming cell (PFC) response of their spleen cells to TNP-treated aminoethylated polyacrylamide beads. Recovery is presumably the result of repopulation of the peripheral lymphoid system by cells originating in the BM. By enzyme-linked immunosorbent assay (ELISA), and by hapten-augmentable PFC assay, we show that, after recovery from irradiation with their BM shielded, old animals produce low auto-anti-Id responses, like those of young animals. The transfer of splenic T cells into mice irradiated with their BM shielded provided evidence that the magnitude of the auto-anti-Id response is controlled by the peripheral T cells. Thus, mice that received splenic T cells from aged donors produced high levels of auto-anti-Id while those that received splenic T cells from young donors produce low levels of auto-anti-Id.
用三硝基苯基(TNP)- 聚蔗糖免疫小鼠后,小鼠产生了抗TNP抗体以及针对抗TNP抗体的自身抗独特型(自身抗Id)抗体。年龄较大的动物产生的自身抗Id比年幼动物更多。当小鼠在其骨髓(BM)部分受到屏蔽的情况下接受正常致死剂量的辐射时,它们存活下来并在缓慢地(6周)恢复免疫功能,这可通过其脾脏中有核细胞的数量以及其脾细胞对TNP处理的氨乙基化聚丙烯酰胺珠的体外原发性空斑形成细胞(PFC)反应来表明。恢复大概是起源于BM的细胞对外周淋巴系统进行重新填充的结果。通过酶联免疫吸附测定(ELISA)以及半抗原增强的PFC测定,我们表明,在其BM受到屏蔽的辐射后恢复过来的老年动物产生低水平的自身抗Id反应,类似于年幼动物的反应。将脾T细胞转移到其BM受到屏蔽的辐射小鼠体内提供了证据,表明自身抗Id反应的强度受外周T细胞控制。因此,接受老年供体脾T细胞的小鼠产生高水平的自身抗Id,而接受年轻供体脾T细胞的小鼠产生低水平的自身抗Id。