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Gene Review

Klra8  -  killer cell lectin-like receptor,...

Mus musculus

Synonyms: Cmv-1, Cmv1, Killer cell lectin-like receptor 8, Ly-49h, Ly49-h, ...
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Disease relevance of Klra8

  • Natural resistance to infection with mouse cytomegalovirus (MCMV) is controlled by a dominant locus, Cmv1 [1].
  • Transgenic expression of the activating natural killer receptor Ly49H confers resistance to cytomegalovirus in genetically susceptible mice [1].
  • Although there is a similar hierarchy of resistance to MCMV and HSV-1 with respect to the C57BL and BALB genetic backgrounds, the strain distribution pattern of HSV-1 replication in recombinant inbred mice suggests that Cmv-1 is not involved in restricting the spread of this virus [2].
  • As these lack the Cmv1 gene, which provides a protective natural killer (NK) cell response in C57BL congenic mice, the C57BL background may carry a pancreatitis susceptibility gene able to counter NK-mediated restriction of viral replication [3].

High impact information on Klra8

  • Susceptibility to infection with MCMV is controlled by Cmv1, a chromosome 6 locus that regulates natural killer (NK) cell activity against virally infected targets [4].
  • The recombinant inbred strain BXD-8/Ty (BXD-8; ref. 18), derived from Cmv1r C57BL/6 (B6, resistant) and Cmv1s DBA/2 (susceptible), is of particular interest because it is highly susceptible to MCMV infection despite having a B6 haplotype at Cmv1 [4].
  • TLR9-mediated cytokine secretion promotes viral clearance by NK cells that express the MCMV-specific receptor Ly49H [5].
  • While some studies localized Cmv1 as distal to the Ly49 gene cluster, genetic and functional analysis identified Ly49h as a pivotal factor in resistance to MCMV [1].
  • Our results are discussed in relation to recent reports demonstrating that innate resistance to MCMV requires the presence of NK cells expressing the KARAP/DAP12-associated receptor Ly49H [6].

Chemical compound and disease context of Klra8


Biological context of Klra8

  • For this, a total of 45 DNA markers corresponding to either cloned genes or microsatellites were mapped within a 7.9-cM interval overlapping the Cmv1 region [8].
  • In our effort to clone Cmv1, we have constructed a high-resolution genetic linkage map in the proximity of the gene [8].
  • To narrow the Cmv1 critical region, we developed novel NKC genetic markers and used these to genotype informative backcross and intra-NKC recombinant congenic mouse DNA samples [9].
  • This high resolution, integrated physical and genetic NKC map will facilitate identification of Cmv1 and other NKC-linked loci that regulate NK cell-mediated immunity [9].
  • The Cmv1 phenotypes of mice recombinant in this interval were tested by infection with MCMV [10].

Associations of Klra8 with chemical compounds

  • In this regard, NKG2D and Ly49H lectin-like molecules trigger NK-cell functions recognizing, respectively class I-related stress-inducible molecules and the m157 murine CMV glycoprotein [11].
  • In addition, we show that a second Ly49 family member that lacks an immunoreceptor tyrosine-based inhibitory motif and contains a charged residue in the transmembrane domain, Ly49H, also associates with DAP12 [12].

Other interactions of Klra8

  • NKC species conservation suggests that the human NKC may contain orthologues for the mouse viral disease resistance genes, Cmv1 and Rmp1 [13].
  • This result excludes Cd94 and Nkg2d as candidates whereas it localizes the Ly49 genes within the minimal genetic interval for Cmv1 [14].
  • Two of these genes, Ly49h and i, are very closely related to the well characterized Ly49c gene in the carbohydrate recognition domain [15].
  • In adult C57BL/6 mice, the control of MCMV in the spleen is mediated by a perforin-dependent mechanism, regulated in part by the Cmv-1 gene, which maps closely to the Ly49 family [16].
  • Our recent genetic analysis of backcross mice demonstrated that the NK gene complex (NKC)-linked Cmv1 locus should reside between the Ly49 and Prp gene clusters on distal mouse chromosome 6 [9].

Analytical, diagnostic and therapeutic context of Klra8


  1. Transgenic expression of the activating natural killer receptor Ly49H confers resistance to cytomegalovirus in genetically susceptible mice. Lee, S.H., Zafer, A., de Repentigny, Y., Kothary, R., Tremblay, M.L., Gros, P., Duplay, P., Webb, J.R., Vidal, S.M. J. Exp. Med. (2003) [Pubmed]
  2. Cmv-1, a genetic locus that controls murine cytomegalovirus replication in the spleen. Scalzo, A.A., Fitzgerald, N.A., Simmons, A., La Vista, A.B., Shellam, G.R. J. Exp. Med. (1990) [Pubmed]
  3. Factors influencing the effects of murine cytomegalovirus on the pancreas. Price, P., Baxter, A.G., Allcock, R.N., Papadimitriou, J.M. Eur. J. Clin. Invest. (1998) [Pubmed]
  4. Susceptibility to mouse cytomegalovirus is associated with deletion of an activating natural killer cell receptor of the C-type lectin superfamily. Lee, S.H., Girard, S., Macina, D., Busà, M., Zafer, A., Belouchi, A., Gros, P., Vidal, S.M. Nat. Genet. (2001) [Pubmed]
  5. TLR9-dependent recognition of MCMV by IPC and DC generates coordinated cytokine responses that activate antiviral NK cell function. Krug, A., French, A.R., Barchet, W., Fischer, J.A., Dzionek, A., Pingel, J.T., Orihuela, M.M., Akira, S., Yokoyama, W.M., Colonna, M. Immunity (2004) [Pubmed]
  6. Pivotal role of KARAP/DAP12 adaptor molecule in the natural killer cell-mediated resistance to murine cytomegalovirus infection. Sjölin, H., Tomasello, E., Mousavi-Jazi, M., Bartolazzi, A., Kärre, K., Vivier, E., Cerboni, C. J. Exp. Med. (2002) [Pubmed]
  7. Murine cytomegalovirus m157 mutation and variation leads to immune evasion of natural killer cells. Voigt, V., Forbes, C.A., Tonkin, J.N., Degli-Esposti, M.A., Smith, H.R., Yokoyama, W.M., Scalzo, A.A. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  8. High-resolution linkage map in the proximity of the host resistance locus Cmv1. Depatie, C., Muise, E., Lepage, P., Gros, P., Vidal, S.M. Genomics (1997) [Pubmed]
  9. Localization on a physical map of the NKC-linked Cmv1 locus between Ly49b and the Prp gene cluster on mouse chromosome 6. Brown, M.G., Zhang, J., Du, Y., Stoll, J., Yokoyama, W.M., Scalzo, A.A. J. Immunol. (1999) [Pubmed]
  10. The Cmv1 host resistance locus is closely linked to the Ly49 multigene family within the natural killer cell gene complex on mouse chromosome 6. Forbes, C.A., Brown, M.G., Cho, R., Shellam, G.R., Yokoyama, W.M., Scalzo, A.A. Genomics (1997) [Pubmed]
  11. Natural killer cell receptors for major histocompatibility complex class I and related molecules in cytomegalovirus infection. López-Botet, M., Angulo, A., Gumá, M. Tissue Antigens (2004) [Pubmed]
  12. Induction of DAP12 phosphorylation, calcium mobilization, and cytokine secretion by Ly49H. Gosselin, P., Mason, L.H., Willette-Brown, J., Ortaldo, J.R., McVicar, D.W., Anderson, S.K. J. Leukoc. Biol. (1999) [Pubmed]
  13. A 2-Mb YAC contig and physical map of the natural killer gene complex on mouse chromosome 6. Brown, M.G., Fulmek, S., Matsumoto, K., Cho, R., Lyons, P.A., Levy, E.R., Scalzo, A.A., Yokoyama, W.M. Genomics (1997) [Pubmed]
  14. Assessment of Cmv1 candidates by genetic mapping and in vivo antibody depletion of NK cell subsets. Depatie, C., Chalifour, A., Paré, C., Lee, S.H., Vidal, S.M., Lemieux, S. Int. Immunol. (1999) [Pubmed]
  15. Localization of five new Ly49 genes, including three closely related to Ly49c. McQueen, K.L., Freeman, J.D., Takei, F., Mager, D.L. Immunogenetics (1998) [Pubmed]
  16. The role of LY49 NK cell subsets in the regulation of murine cytomegalovirus infections. Tay, C.H., Yu, L.Y., Kumar, V., Mason, L., Ortaldo, J.R., Welsh, R.M. J. Immunol. (1999) [Pubmed]
  17. Critical Residues at the Ly49 Natural Killer Receptor's Homodimer Interface Determine Functional Recognition of m157, a Mouse Cytomegalovirus MHC Class I-Like Protein. Kielczewska, A., Kim, H.S., Lanier, L.L., Dimasi, N., Vidal, S.M. J. Immunol. (2007) [Pubmed]
  18. Sequence-ready BAC contig, physical, and transcriptional map of a 2-Mb region overlapping the mouse chromosome 6 host-resistance locus Cmv1. Depatie, C., Lee, S.H., Stafford, A., Avner, P., Belouchi, A., Gros, P., Vidal, S.M. Genomics (2000) [Pubmed]
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