Influence of H–2 complex on acquired resistance to Leishmania donovani infection in mice

Publisher Website
Google Scholar
Abstract
Innate susceptibility to Leishmania donovani infection in mice (measured over 2–4 weeks) is under the control of a single autosomal gene (Lsh) segregating for incompletely dominant resistant (r) and recessive susceptible (s) alleles1. This locus maps2 away from the known histocompatibility loci to a position between the centromere and Id–1 on the chromosome 1 of the mouse. Amongst homozygous recessive Lshs strains of mice two patterns of recovery are observed3 when the course of infection is followed over a longer term. In some strains a dramatic fall in parasite numbers with histological liver damage occurs while other strains maintain immense parasite loads for up to two years involving mononuclear phagocytes throughout the body. We now present evidence which suggests that this difference in long-term response is largely controlled by a gene(s) within, or closely adjacent to, the major histocompatibility complex (H–2) of the mouse.

This publication has 11 references indexed in Scilit: