GENETIC CONTROL OF THE ANTIBODY RESPONSE TO MICROBIAL ANTIGENS

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RIIIS/J mice lack an autosomal dominant gene(s) that influences the magnitude of the antibody response to several bacterial polysaccharide antigens. Low responsiveness is demonstrable, whether or not polysaccharide is administered as a helper T cell-independent antigen or as a helper T cell-dependent antigen conjugated to an immunogenic carrier; however, RIIIS/J mice make good anti-hapten antibody responses to haptenated polysaccharides. The low antibody response of RIIIS/J mice to Type Ill pneumococcal polysaccharide (SSS-III) does not appear to be due to an imbalance in the activity of regulatory T lymphocytes. In comparison to other strains of mice, RIIIS/J mice elicit low antibody responses to bacterial lipopolysaccharide (LPS). They do not develop a cyclic primary antibody response or a secondary antibody response to LPS: the latter is not due to the lack of a mitogenic response to LPS. They also produce auto-anti-idiotypic antibody after immunization with TNP-Ficoll.