Chromosomes X, 9, and the H2 locus interact epistatically to control Leishmania major infection.
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.
Roberts
L J
LJ
The Walter and Eliza Hall Institute of Medical Research, Victoria, Australia.
Baldwin
T M
TM
Speed
T P
TP
Handman
E
E
Foote
S J
SJ
D000818:Animals; D000913:Antibodies, Protozoan / Q000096:biosynthesis; D002874:Chromosome Mapping; D002875:Chromosomes / Q000276:immunology*; D005260:Female; D005805:Genes, MHC Class I; D006183:H-2 Antigens / Q000235:genetics*; D018320:Leishmania major / Q000276:immunology*; D016773:Leishmaniasis, Cutaneous / Q000235:genetics*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018417:Th1 Cells / Q000276:immunology
D000913:Antibodies, Protozoan; D006183:H-2 Antigens