Blackwell J, Freeman J, Bradley D
Nature. 1980 Jan 3;283(5742):72-4. doi: 10.1038/283072a0.
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) alleles. This locus maps 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 Lsh strains of mice two patterns of recovery are observed 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.
小鼠对杜氏利什曼原虫感染的先天易感性（在2至4周内测定）受单个常染色体基因（Lsh）控制，该基因分离出不完全显性抗性（r）和隐性易感（s）等位基因。该基因座位于已知组织相容性基因座之外，位于小鼠1号染色体着丝粒和Id-1之间的位置。在纯合隐性Lsh小鼠品系中，当长期跟踪感染过程时，观察到两种恢复模式。在一些品系中，寄生虫数量急剧下降并伴有肝脏组织学损伤，而其他品系在长达两年的时间内维持大量寄生虫负荷，全身单核吞噬细胞均受累。我们现在提供的证据表明，这种长期反应的差异在很大程度上受小鼠主要组织相容性复合体（H-2）内部或与其紧密相邻的一个基因或多个基因控制。
