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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Central role for type I interferons and Tyk2 in lipopolysaccharide-induced endotoxin shock.

Toll-like receptor-4 activation by lipopolysaccharide (LPS) induces the expression of interferon-beta (IFN-beta) in a MyD88-independent manner. Here we report that mice devoid of the JAK protein tyrosine kinase family member, Tyk2, were resistant to shock induced by high doses of LPS. Basal and LPS-induced expression of IFN-beta and IFN-alpha4 mRNA in Tyk2-null macrophages were diminished. However, Tyk2-null mice showed normal systemic production of nitric oxide and proinflammatory cytokines and the in vivo response to tumor necrosis factor (TNF) was unperturbed. IFN-beta-null but not STAT1-null mice were also resistant to high dose LPS treatment. Together, these data suggest that Tyk2 and IFN-beta are essential effectors in LPS induced lethality.[1]


  1. Central role for type I interferons and Tyk2 in lipopolysaccharide-induced endotoxin shock. Karaghiosoff, M., Steinborn, R., Kovarik, P., Kriegshäuser, G., Baccarini, M., Donabauer, B., Reichart, U., Kolbe, T., Bogdan, C., Leanderson, T., Levy, D., Decker, T., Müller, M. Nat. Immunol. (2003) [Pubmed]
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