Rowley D A, Griffith P, Lorbach I
J Exp Med. 1981 Jun 1;153(6):1377-90. doi: 10.1084/jem.153.6.1377.
A/He mice actively producing complementary or anti-idiotypic antibody directed against a combining site structure for phosphorylcholine (PC) have profound and long-lasting suppression of their response to PC. B cells from unresponsive mice are unresponsive in vitro, and attempts to demonstrate suppressor cells in unresponsive mice were unsuccessful. Although the process ultimately responsible for suppression has not been defined, suppression can be initiated by anti-idiotypic antibody alone and prevented by complementary Ig; i.e., by anti-PC antibody. Furthermore, a suppressed anti-PC response can be rescued by sublethal irradiation and anti-PC antibody given passively. The recovery of the suppressed response is slow and presumably results from maturation from "stem" cells, which are protected from tolerization by the passively given antibody. Thus, by extrapolation, one of the functions of secreted Ig may be to protect the clone that produces it.
主动产生针对磷酸胆碱（PC）结合位点结构的互补抗体或抗独特型抗体的A/He小鼠，对PC的反应受到深刻且持久的抑制。无反应小鼠的B细胞在体外无反应，且试图在无反应小鼠中证明抑制细胞的尝试未成功。尽管最终导致抑制的过程尚未明确，但抑制可仅由抗独特型抗体引发，并可被互补Ig（即抗PC抗体）阻止。此外，经亚致死剂量照射并被动给予抗PC抗体后，受抑制的抗PC反应可得到挽救。受抑制反应的恢复缓慢，推测是由“干细胞”成熟所致，这些干细胞因被动给予的抗体而免受耐受形成的影响。因此，由此推断，分泌型Ig的功能之一可能是保护产生它的克隆。
