A high-titre IgE-antibody response to Schistosoma japonicum antigen (Sj) is obtained if helper T cells are appropriately induced by the infection. The antibody responses were found to be regulated by a gene(s) linked to the major histocompatibility complex. Strains of H-2a and H-2k haplotypes were high responders, whereas H-2d, H-2b and H-2s strains were not. Results obtained by using intra-H-2 recombinant strains suggested that the immune-response (Ir) gene was mapped in the I-E subregion, although a possibility of the presence of complementary genes was not excluded. Interestingly, in low responders such as BALB/c mice, Sj-specific carrier effect could be demonstrated when mice were infected with S. japonicum before challenge immunization with dinitrophenylated Sj (DNP-Sj). Moreover, BALB/c as well as C3H/He was a high responder to Sj in proliferation of peritoneal exudate T-lymphocyte enriched cells in vitro, whereas B10.S was not. Based on these observations, possible roles of Ir genes in immune responses to Sj are discussed.
The antigenicity of Trichomonas vaginalis to elicit IgE antibody was examined in mice. The soluble antigen was prepared by sonication of in vitro cultured T. vaginalis lines. BALB/c mice were immunized by various doses of the antigen with alum followed by a booster injection on day 14 after primary injection of the protozoan antigen. The highest IgE antibody titer was found in mice immunized with 30 μg of the antigen. The IgE antibody response to Trichomonas antigen is regulated by at least two immune response genes: one localized in the I region (K to I-B subregions) of chromosome 17, the other in a not yet identified chromosome.
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