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The immune response to the random linear terpolymer of L-glutamic acid, L-lysine, and L-phenylalanine (GLphi) is under dominant H-2-linked Ir gene control in the mouse. Matings between two nonresponder strains produced responder F1 hybrids, demonstrating complementation of the nonresponder alleles. This observation, coupled with the fact that several intra H-2 recombinant strains derived by recombination between two nonresponder parental haplotypes are also GLphi responders, indicated at least two dominant loci are concerned with responsiveness to this terpolymer. The complementary genes were termed alpha (tentatively localized in a new subregion of the H-2 complex, I-F) and beta, which maps in the I-A subregion. Generally, both the alpha(+) and beta(+) alleles are required for responsiveness. However, in the (C57BL/6J X SJL)F1 hybrid we noted complementation between two parental nonresponder strains, each of which carried beta genes derived from different H-2 haplotypes, yet lacked functional alpha genes. The possible cell levels at which these genes may function in the regulation of the immune response are discussed.

Complementation of H-2-linked Ir genes in the mouse.