Chiorazzi N, Tung A S, Katz D H
J Exp Med. 1977 Jul 1;146(1):302-7. doi: 10.1084/jem.146.1.302.
Mice of the inbred strains, C57BL/6 and C57BL/10 (H-2b), are genetically incapable of developing IgE antibody responses to ragweed pollen extract (RE) or its dinitrophenylated derivative, DNP-RE. This nonresponsiveness has previously been thought to reflect the absence of a relevant H-2-linked Ir genes controlling responses of inbred mice to these antigens. However, pretreatment of H-2b mice with either low doses of ionizing X irradiation or cyclophosphamide abrogates the nonresponder status of such animals, apparently by removal of a suppressive mechanism normally inhibiting development of IgE responses to these antigens. The implications of these findings for mechanisms of genetic control of IgE antibody synthesis and the Ir-gene concept are discussed.
近交系C57BL/6和C57BL/10（H-2b）小鼠在基因上无法对豚草花粉提取物（RE）或其二硝基苯基化衍生物DNP-RE产生IgE抗体反应。以前认为这种无反应性反映了缺乏控制近交系小鼠对这些抗原反应的相关H-2连锁Ir基因。然而，用低剂量的电离X射线或环磷酰胺对H-2b小鼠进行预处理，可消除此类动物的无反应状态，显然是通过去除通常抑制对这些抗原产生IgE反应的抑制机制来实现的。讨论了这些发现对IgE抗体合成的遗传控制机制和Ir基因概念的意义。
