Sapin C, Hirsch F, Delaporte J P, Bazin H, Druet P
Immunogenetics. 1984;20(3):227-36. doi: 10.1007/BF00364205.
An autoimmune disease and a dramatic increase in total serum IgE concentration are observed in BN rats that are chronically injected with HgCl2. In contrast, LEW rats do not develop the characteristic glomerulonephritis and are very "low IgE responders". In this study, we examined the genetic control of total serum IgE increase after HgCl2 injection in F1 and F2 hybrids, in both backcrosses between LEW and BN rats, and in LEW.1N congenic rats. Genetic analysis was performed using peak IgE concentrations expressed as log microgram/ml. A high IgE phenotype was found to be dominant. Eighty-five percent of F2 variance was due to genetic factors (VG) while only 15% of this variance was caused by environmental factors (VE). From observations in F2 hybrids and backcrosses, estimations of additive variance (VA) and dominance variance (VD) were made following three different methods. Genetic control by about four loci is demonstrated. One of these genes is RT1-linked. This gene contributes to 25% of the phenotypic difference observed between BN and LEW rats. No correlation was found between the peak total IgE level and autoimmune disease based on IgG deposition in spleen and/or kidney.
在长期注射氯化汞的BN大鼠中观察到自身免疫性疾病和血清总IgE浓度显著升高。相比之下，LEW大鼠不会发展出特征性的肾小球肾炎，并且是非常“低IgE反应者”。在本研究中，我们检测了F1和F2杂种、LEW和BN大鼠的两个回交群体以及LEW.1N同源基因大鼠在注射氯化汞后血清总IgE升高的遗传控制情况。使用以对数微克/毫升表示的IgE峰值浓度进行遗传分析。发现高IgE表型是显性的。F2代的85%的变异是由遗传因素（VG）引起的，而只有15%的变异是由环境因素（VE）导致的。根据对F2杂种和回交群体的观察，采用三种不同方法对加性方差（VA）和显性方差（VD）进行了估计。证实了约四个基因座的遗传控制。其中一个基因与RT1连锁。该基因导致BN和LEW大鼠之间观察到的表型差异的25%。基于脾脏和/或肾脏中IgG沉积，未发现总IgE峰值水平与自身免疫性疾病之间存在相关性。
