Strayer D S, Lee W M, Rowley D A, Köhler H
J Immunol. 1975 Feb;114(2 pt 2):728-33.
We have examined the ability of anti-receptor antibody (ARA) to induce specific unresponsiveness to the hapten, phosphorylcholine (PC), in neonatal and adult mice. When ARA is given to adult mice, suppression is of short duration. Cells from such mice are responsive in vitro, indicating that suppression in vivo is probably due to blockade of receptors by persisting ARA. ARA given to neonatal mice induces long-term unresponsiveness. The mice apparently have decreased numbers of PC-responsive cells, since cells from such mice are unresponsive both in vitro and in adoptive transfer. Furthermore, cells from neonatally suppressed animals do not suppress the response of normal cells either in vitro or in adoptive transfer, indicating that unresponsiveness is most likely not due to active suppression. We therefore conclude that ARA given to neonates depletes the clone of receptor-bearing cells at the time ARA is given. Clonal depletion may result from antibody-dependent cell mediated cytotoxicity.
我们研究了抗受体抗体(ARA)诱导新生小鼠和成年小鼠对半抗原磷酰胆碱(PC)产生特异性无反应性的能力。将ARA给予成年小鼠时,抑制作用持续时间较短。来自此类小鼠的细胞在体外有反应,这表明体内抑制可能是由于持续存在的ARA阻断了受体。将ARA给予新生小鼠会诱导长期无反应性。这些小鼠中PC反应性细胞的数量明显减少,因为来自此类小鼠的细胞在体外和过继转移中均无反应。此外,来自新生期受抑制动物的细胞在体外或过继转移中均不抑制正常细胞的反应,这表明无反应性很可能不是由于主动抑制。因此,我们得出结论,在给予ARA时,给予新生小鼠的ARA会耗尽携带受体的细胞克隆。克隆性耗竭可能是由抗体依赖性细胞介导的细胞毒性导致的。