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Science 11 December 1998:
Vol. 282. no. 5396, pp. 2085 - 2088
DOI: 10.1126/science.282.5396.2085
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Reports

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

Alexander Poltorak, Xiaolong He, * Irina Smirnova, Mu-Ya Liu, dagger Christophe Van Huffel, ddagger Xin Du, Dale Birdwell, Erica Alejos, Maria Silva, Chris Galanos, Marina Freudenberg, Paola Ricciardi-Castagnoli, Betsy Layton, Bruce Beutler §

Mutations of the gene Lps selectively impede lipopolysaccharide (LPS) signal transduction in C3H/HeJ and C57BL/10ScCr mice, rendering them resistant to endotoxin yet highly susceptible to Gram-negative infection. The codominant Lpsd allele of C3H/HeJ mice was shown to correspond to a missense mutation in the third exon of the Toll-like receptor-4 gene (Tlr4), predicted to replace proline with histidine at position 712 of the polypeptide chain. C57BL/10ScCr mice are homozygous for a null mutation of Tlr4. Thus, the mammalian Tlr4 protein has been adapted primarily to subserve the recognition of LPS and presumably transduces the LPS signal across the plasma membrane. Destructive mutations of Tlr4 predispose to the development of Gram-negative sepsis, leaving most aspects of immune function intact.

A. Poltorak, X. He, I. Smirnova, M.-Y. Liu, C. Van Huffel, X. Du, D. Birdwell, E. Alejos, M. Silva, B. Layton, B. Beutler, Howard Hughes Medical Institute and the Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75235-9050 USA. C. Galanos and M. Freudenberg, Max-Planck Institute für Immunobiologie, Freiburg, Germany. P. Ricciardi, CNR-Cellular and Molecular Pharmacology Center, Milan, Italy.
*   Present address: Northwestern University, 2300 Children's Plaza, No. 209, Chicago, IL 60614-3394, USA.

dagger    Present address: University of Texas Southwestern Medical Center, Department of Pharmacology, Dallas, TX 75235-9041 USA.

ddagger    Present address: Millennium, Inc., Cambridge, MA 02139-4815, USA.

§   To whom correspondence should be addressed at Howard Hughes Medical Institute, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.

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J. Immunol. 179, 8500-8508
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Critical Role of the Phosphatidylinositol 3-Kinase/Akt/Glycogen Synthase Kinase-3 Signaling Pathway in Recovery from Anthrax Lethal Toxin-induced Cell Cycle Arrest and MEK Cleavage in Macrophages.
S.-D. Ha, D. Ng, S. L. Pelech, and S. O. Kim (2007)
J. Biol. Chem. 282, 36230-36239
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The Effect of Altered Toll-like Receptor 4 Signaling on Cancer Cachexia.
T. Y. Cannon, D. Guttridge, J. Dahlman, J. R. George, V. Lai, C. Shores, P. Buzkova, and M. E. Couch (2007)
Arch Otolaryngol Head Neck Surg 133, 1263-1269
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Transgenic Expression of Bcl-xL or Bcl-2 by Murine B Cells Enhances the In Vivo Antipolysaccharide, but Not Antiprotein, Response to Intact Streptococcus pneumoniae.
G. Chattopadhyay, A. Q. Khan, G. Sen, J. Colino, W. duBois, A. Rubtsov, R. M. Torres, M. Potter, and C. M. Snapper (2007)
J. Immunol. 179, 7523-7534
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Soluble CD14 Discriminates Slight Structural Differences between Lipid As That Lead to Distinct Host Cell Activation.
Y. Asai, Y. Makimura, A. Kawabata, and T. Ogawa (2007)
J. Immunol. 179, 7674-7683
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Membrane Vesicles Are Immunogenic Facsimiles of Salmonella typhimurium That Potently Activate Dendritic Cells, Prime B and T Cell Responses, and Stimulate Protective Immunity In Vivo.
R. C. Alaniz, B. L. Deatherage, J. C. Lara, and B. T. Cookson (2007)
J. Immunol. 179, 7692-7701
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Activation of Protein Kinase D1 in Mast Cells in Response to Innate, Adaptive, and Growth Factor Signals.
T. R. Murphy, H. J. Legere III, and H. R. Katz (2007)
J. Immunol. 179, 7876-7882
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