Kenny J J, Guelde G, Claflin J L, Scher I
J Immunol. 1981 Oct;127(4):1629-33.
The x-linked CBA/N defect results in an altered idiotype expression among the anti-phosphocholine (PC) antibodies produced after antigenic challenge with the thymic dependent antigen PC-KLH but does not preclude the response to this hapten as previously suggested. The majority of immune-defective F1 male mice can be divided into 2 groups based on their T15 idiotype profile. Group 1 mice fail to produce anti-PC antibodies bearing the T15 idiotype in either a primary or secondary response, whereas group 2 mice produce low levels of T15 idiotype; however, this idiotype often appears only after secondary immunization. These responses are distinct from the anti-PC response of normal F1 females, which is predominantly of the T15 idiotype. In addition to the altered idiotype expression, F1 male mice exhibited a greatly reduced primary anti-PC response compared to normal mice, and secondary responses were approximately one-third that of normal mice. The delayed expression of anti-PC antibodies in immune defective mice appears to be due to their inability to produce IgM anti-PC antibodies in either a primary or secondary response to PC-KLH.
X连锁的CBA/N缺陷导致在用胸腺依赖性抗原PC-KLH进行抗原刺激后产生的抗磷酸胆碱（PC）抗体中独特型表达发生改变，但并不像之前所认为的那样排除对这种半抗原的反应。大多数免疫缺陷的F1雄性小鼠可根据其T15独特型谱分为两组。第1组小鼠在初次或二次反应中均不能产生带有T15独特型的抗PC抗体，而第2组小鼠产生低水平的T15独特型；然而，这种独特型通常仅在二次免疫后出现。这些反应不同于正常F1雌性小鼠的抗PC反应，后者主要为T15独特型。除了独特型表达改变外，F1雄性小鼠与正常小鼠相比，初次抗PC反应大大降低，二次反应约为正常小鼠的三分之一。免疫缺陷小鼠中抗PC抗体的延迟表达似乎是由于它们在对PC-KLH的初次或二次反应中无法产生IgM抗PC抗体。
