The immune response to bacteriophage fd has been tested in congenic resistant strains of mice. B10 mice are high responders; B10.BR and B10.D2 mice are low responders. B10.A mice with the recombinant H-2a haplotype as well as heterozygous H-2k/d (B10.BR × B10.D2) F1 mice respond with high antibody titers, indicating the existence of two complementing Ir genes. From the results obtaiend with recombinant and F1 hybrid mice, Irfdα can be localized to the right of the crossover between the IE and IC subregions, Irfdα to the left of IB, presumably at IA. Complementation is observed with selected pairs of alleles only, suggesting α-β coupled complementation.

Low responsiveness of B10.A(2R) and (B10.A × B10.A(2R)) F1 mice is caused by a specific suppressor gene located at the Db subregion. This suppressor gene is active only with selected Irfdβ alleles.

In addition to genes in the H-2 complex, there are non-H-2 background genes modulating H-2 regulated anti-fd response.

B10.BR mice lack primary IgM and IgG antibodies, yet are able to mount a secondary IgG anti-fd response, giving evidence for intact memory formation in this low responder strain.

The combined data are most easily interpreted by assuming that both H-2 and non-H-2-genes modulate the effective immunogenic dose of antigen.

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This work was supported by the Schwerpunktsprogramm “Physiologie und Pathophysiologie des Immunsystems” of the Deutsche Forschungsgemeinschaft with Grant Ko 379/8 to E.K. and by Grant Fa 71/4 to F.F.

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