DESCRIPTION:

QTL associated with cytomegalovirus resistance 3. The confidence interval is Chr6:128784912-137388450 bp,+strand

LABEL:

QTL-Cmv3-Mouse-Chr 6

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2024-10-22

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:3574425

AUTHORS:

Desrosiers MP, Kielczewska A, Loredo-Osti JC, Adam SG, Makrigiannis AP, Lemieux S, Pham T, Lodoen MB, Morgan K, Lanier LL, Vidal SM

TITLE:

Epistasis between mouse Klra and major histocompatibility complex class I loci is associated with a new mechanism of natural killer cell-mediated innate resistance to cytomegalovirus infection.

JOURNAL:

Nature genetics Jun 2005, Vol 37, pp. 593-9

ABSTRACT:

Experimental infection with mouse cytomegalovirus (MCMV) has been used to elucidate the intricate host-pathogen mechanisms that determine innate resistance to infection. Linkage analyses in F(2) progeny from MCMV-resistant MA/My (H2 (k)) and MCMV-susceptible BALB/c (H2 (d)) and BALB.K (H2 (k)) mouse strains indicated that only the combination of alleles encoded by a gene in the Klra (also called Ly49) cluster on chromosome 6, and one in the major histocompatibility complex (H2) on chromosome 17, is associated with virus resistance. We found that natural killer cell-activating receptor Ly49P specifically recognized MCMV-infected cells, dependent on the presence of the H2 (k) haplotype. This binding was blocked using antibodies to H-2D(k) but not antibodies to H-2K(k). These results are suggestive of a new natural killer cell mechanism implicated in MCMV resistance, which depends on the functional interaction of the Ly49P receptor and the major histocompatibility complex class I molecule H-2D(k) on MCMV-infected cells. PUBMED: 15895081
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