Augmentation of the antibody response by hapten help: I. Dominant genetic control

The objective of the present work was to characterize those genetic factors that determine susceptibility to “hapten help,” i.e., the augmentation of B-cell responses by hapten-reactive T cells. After mice had been sensitized to the hapten azobenzenearsonate (ABA), one of two approaches was used to assay hapten help. In the first, circumvention of tolerance to low doses of bovine γ-globulin (BGG) was augmented in CBA but not in C57BL/6 mice, as measured by serum anti-BGG antibody after challenge with ABA-BGG. Second, similar strain differences but on a larger scale were demonstrated in the anti-BGG plaque-forming cell (PFC) response of spleen cells from hapten-primed nontolerized mice after challenge with ABA-BGG. Results with the F1-hybrid of a cross between a high responder and a low responder for hapten help demonstrated that high responsiveness is dominant. Experiments with recombinant inbred mice from high- and low-responder progenitor strains suggested that hapten help is associated not with the major histocompatibility complex (H-2) so much as with minor histocompatibility antigens such as H-22 and/or H-24, both of which are on chromosome 7.