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Leishmania donovani infection in heterozygous and recombinant H-2 haplotype mice

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Abstract

On a B10 (Lsh s) 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-2 s, H-2 r), “cure” (H-2 b) and “noncure” (H-2 d, H-2 q, H-2 f), with cure behaving as a recessive trait in H-2 b/H-2 d 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-2 k 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.

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Blackwell, J.M. Leishmania donovani infection in heterozygous and recombinant H-2 haplotype mice. Immunogenetics 18, 101–109 (1983). https://doi.org/10.1007/BF00368537

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  • DOI: https://doi.org/10.1007/BF00368537

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