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Genetic control of the immune response to (T,G)-A--L in C3H in equilibrium C57 tetraparental mice
Authors:K B Bechtol  T G Wegmann  J H Freed  F C Grumet  B W Chesebro  L A Herzenberg  H O McDevitt
Institution:1. Departments of Medicine (Immunology) and Genetics, Stanford University School of Medicine, Stanford, California 94305 U.S.A.;2. Departments of Medicine (Immunology) and Genetics, Biological Laboratories, Harvard University, Cambridge, Massachusetts 02138 U.S.A.
Abstract:When 15 C3H ? C57 tetraparental (allophenic) mice were analyzed for coat color, hemoglobin, and immunoglobulin allotype, all but two were shown to be chimeric. These 15 tetraparental mice were immunized with the synthetic polypeptide (T,G)-A--L, and the origin of the (T,G)-A--L-specific antibody produced was determined by using genetic markers (allotypes) on the immunoglobulin heavy chain constant region. Five tetraparental mice were high responders to (T,G)-A--L and had significant amounts of a (low responder) allotype antibody in their total serum. Three of these mice had significant amounts of anti-(T,G)-A--L antibody of the a (low responder) allotype. The antigen binding capacities of the a allotype fractions of these three were 4–5 times higher than the antigen binding capacities of immunized C3H (low responder) control mice. These results are compatible with the hypothesis that the inability of low-responder mice to produce significant amounts of anti-(T,G)-A--L antibody is a function of Ir-1A gene expression at the level of T cells.
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