Genetic Control of the Antibody Response to Simple Haptens in Congenic Strains of Mice

Abstract

The antibody response to the 2,4,6-trinitrophenyl hapten (TNP) conjugated to mouse serum albumin (MSA) was found to be substantially regulated by products of alleles of the H-2 locus. Mice from each of five strains representing congenic pairs differing at the H-2 and H-3 loci and their F₁ and F₂ progenies were tested. These mice were immunized with a variety of haptens coupled to MSA and their antibody responses were determined after individual serial bleedings by a sensitive test for antigen-binding capacity. The A/Jax and B10.A (H-2^a) strains regularly showed a low antibody response whereas their congenic partners, A.BY and C57BL/10 (H-2^b) gave a markedly higher response to TNP at all times tested. F₁ hybrid progeny gave a low response similar to the H-2^a parent strain. The antibody responses of F₂ mice were consistent with the segregation of the histocompatability alleles as determined by skin transplants. These results support the hypothesis that low antibody responsiveness to the TNP hapten is determined by the H-2^a allele as a dominant trait, whereas homozygosity for the H-2^b allele leads to high responsiveness even on diverse strain backgrounds.