GENETIC CONTROL OF THE ANTIBODY RESPONSE TO MICROBIAL ANTIGENS

RIIIS/J小鼠缺乏影响免疫应答的常染色体显性基因。 对几种细菌多糖的抗体应答的幅度 抗原低反应性是明显的，无论是否是多糖 作为辅助T细胞非依赖性抗原或辅助T细胞非依赖性抗原施用。 与免疫原性载体缀合的细胞依赖性抗原;然而， RIIIS/J小鼠对半抗原抗体产生良好的抗半抗原抗体应答。 多糖RIIIS/J小鼠对III型抗体的低应答 肺炎球菌多糖（SSS-III）似乎不是由于 调节性T淋巴细胞活性失衡。相比 其他品系的小鼠，RIIIS/J小鼠引起低抗体应答， 细菌脂多糖（LPS）。他们没有发展出一个循环初级 抗体反应或对LPS的二次抗体反应：后者是 而不是由于缺乏对LPS的促有丝分裂反应。它们还产生 用TNP-Ficoll免疫后的自身抗独特型抗体。

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.