Polyclonal IgE increase after H9CI2 injections in BN and LEW rats: A genetic analysis

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Abstract
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 μg/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.