title: Leishmania donovani infection in heterozygous and recombinant H-2 haplotype mice.
abstract: On a B10 (Lshs) genetic background the development of acquired T-cell-mediated immunity to Leishmania donovani infection in mice is under H-2-linked genetic control. Three phenotypic patterns of recovery were previously observed: "early cure" (H-2s, H-2r), "cure" (H-2b) and "noncure" (H-2d, H-2q, H-2f), with cure behaving as a recessive trait in H-2b/H-2d mice. In this study the long-term response to L. donovani is followed over 130 days of infection in eight recombinant haplotype strains and in six further heterozygous haplotype combinations. Noncure in B10.HTG mice, which carry d alleles for loci at the K end and b alleles for loci at the D end of H-2, confirms that H-2-linked genetic control of the acquired response to L. donovani infection is located in the K end. The complex pattern of dominance relationships observed in the additional heterozygous haplotypes studied, the variable phenotypic response of H-2k mice and of recombinant haplotype strains carrying IEk in common, and the differential early curing activity observed in heterozygotes involving the s but not the r early cure haplotype and in recombinant haplotype mice carrying s alleles to the left of IE suggest, however, that more than one subregion (IE and presumably IA) are involved. Results are interpreted in the light of immunoregulatory T-cell populations previously demonstrated in noncure, cure, and early cure strains.
mesh_terms: D000818:Animals; D006183:H-2 Antigens / Q000235:genetics*; D006579:Heterozygote; D007111:Immunity, Cellular; D007891:Leishmania / Q000472:pathogenicity; D007898:Leishmaniasis, Visceral / Q000235:genetics / Q000276:immunology*; D008099:Liver / Q000469:parasitology; D008285:Major Histocompatibility Complex; D051379:Mice; D008815:Mice, Inbred Strains; D013045:Species Specificity; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D006183:H-2 Antigens