Chromosomes X, 9, and the H2 locus interact epistatically to control Leishmania major infection.

Roberts LJ, Baldwin TM, Speed TP, Handman E, Foote SJ
Eur J Immunol. 1999 29 (9): 3047-50

PMID: 10508279 · DOI:10.1002/(SICI)1521-4141(199909)29:09<3047::AID-IMMU3047>3.0.CO;2-L

As in other infectious diseases, the outcome of a Leishmania major infection is closely tied to the T helper cell response type; progressive disease is associated with a predominant Th2 lymphocyte response, healing with a Th1 response. In mice, susceptibility is genetically con trolled, with BALB/c (C) mice being susceptible and C57BL/6 (B) mice being resistant. Using a genome-wide scan on two large populations of F2 mice created from these strains, we have shown previously that susceptibility to infection with L. major is controlled by two autosomal loci: lmr1 at the H2 locus, and lmr2 on chromosome 9. Employing a strategy to identify loci that interact, we show here that lmr1 and lmr2 interact synergistically, and we describe a new locus lmr3, lying on the X chromosome, whose effect depends on a specific lmr1 haplotype.

MeSH Terms (14)

Animals Antibodies, Protozoan Chromosome Mapping Chromosomes Female Genes, MHC Class I H-2 Antigens Leishmania major Leishmaniasis, Cutaneous Male Mice Mice, Inbred BALB C Mice, Inbred C57BL Th1 Cells

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