| First Author | Qureshi ST | Year | 1999 |
| Journal | Inflamm Res | Volume | 48 |
| Issue | 12 | Pages | 613-20 |
| PubMed ID | 10669111 | Mgi Jnum | J:60495 |
| Mgi Id | MGI:1353376 | Doi | 10.1007/s000110050511 |
| Citation | Qureshi ST, et al. (1999) The Lps locus: genetic regulation of host responses to bacterial lipopolysaccharide. Inflamm Res 48(12):613-20 |
| abstractText | Lipopolysaccharide (LPS), an abundant glycolipid of the outer membrane of gram-negative bacteria, is able to provoke a generalized proinflammatory response in the infected host. Genetic regulation of this trait has been localized to the Lps locus on mouse chromosome 4. Several inbred mouse strains, including C3H/HeJ, C57BL/10ScNCr and C57BL/10ScCr, bear mutations at the Lps locus (Lps(d)) that confer hyporesponsiveness to the immunostimulatory properties of LPS and susceptibility to overwhelming gram-negative bacterial infection. The phenotypic expression of Lps(d) is pleiotropic, affecting several cell types crucial to host defense, including the macrophage. By positional cloning, Toll-like receptor 4 (Tlr4), a transmembrane protein with a cytoplasmic domain that bears homology to the Interleukin-1 receptor, has been identified as the gene encoded by Lps. Tlr4 is a member of a novel gene family that participates in host defense against microbial infection in plants, invertebrates and mammals. Discovery of the molecular basis of the Lps mutation represents a significant advance in defining the fundamental mechanisms of cellular activation by LPS. |
