Owen F L, Nisonoff A
J Exp Med. 1978 Jul 1;148(1):182-94. doi: 10.1084/jem.148.1.182.
Previous reports have shown that suppression of idiotype can be adoptively transferred by T cells, or by rosettes containing T cells with anti-idiotypic receptors, from an idiotypically suppressed, syngeneic mouse. The present data indicate that secondary B cells are highly resistant to such suppression. Priming recipients to the relevant hapten, p-azophenylarsonate, 6 days or 4 mo before the adoptive transfer prevented suppression. This was independent of the carrier used for the hapten group during priming or subsequent immunization, suggesting that resistance to suppression is attributable to secondary cells with specificity for the hapten. The effect of suppressor T cells could also be overcome by mixing them with specifically purified B cells having receptors for the hapten group before the adoptive transfer. Adoptive transfer of the suppressed state by specifically purified B cells from suppressed, hyperimmunized animals confirmed our previous finding that the suppression of idiotype can also be caused by B cells lacking idiotypic receptors, evidently through a mechanism involving clonal dominance. Possible mechanisms of idiotypic suppression by T cells are discussed.
先前的报告显示,同种基因的、受独特型抑制的小鼠的T细胞,或含有带有抗独特型受体的T细胞的玫瑰花结,能够将独特型抑制过继性转移。目前的数据表明,次级B细胞对这种抑制具有高度抗性。在过继性转移前6天或4个月,用相关半抗原对氨基苯砷酸对受体进行致敏可防止抑制作用。这与致敏或后续免疫期间用于半抗原组的载体无关,表明对抑制的抗性归因于对半抗原有特异性的次级细胞。在过继性转移前,将抑制性T细胞与对半抗原有受体的特异性纯化B细胞混合,也可克服抑制性T细胞的作用。从受抑制的、经超免疫的动物中特异性纯化的B细胞对受抑制状态的过继性转移,证实了我们先前的发现,即独特型抑制也可由缺乏独特型受体的B细胞引起,显然是通过一种涉及克隆优势的机制。文中讨论了T细胞进行独特型抑制的可能机制。