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Central role for type I interferons and Tyk2 in lipopolysaccharide-induced endotoxin shock
- Karaghiosoff, M (author)
- Steinborn, R (author)
- Kovarik, P (author)
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- Kriegshauser, G (author)
- Baccarini, M (author)
- Donabauer, B (author)
- Reichart, U (author)
- Kolbe, T (author)
- Bogdan, C (author)
- Levy, D (author)
- Decker, T (author)
- Muller, M (author)
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- (creator_code:org_t)
- 2003-04-07
- 2003
- English.
- In: Nature Immunology. - : Springer Science and Business Media LLC. - 1529-2908 .- 1529-2916. ; 4:5, s. 471-477
- Journal article (peer-reviewed)
Abstract
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- Toll-like receptor-4 activation by lipopolysaccharide (LPS) induces the expression of interferon-P (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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
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- ref (subject category)
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- Karaghiosoff, M
- Steinborn, R
- Kovarik, P
- Kriegshauser, G
- Baccarini, M
- Donabauer, B
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- Reichart, U
- Kolbe, T
- Bogdan, C
- Leanderson, Toma ...
- Levy, D
- Decker, T
- Muller, M
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- Lund University
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