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

Karaghiosoff, M ; Steinborn, R ; Kovarik, P ; Kriegshauser, G ; Baccarini, M ; Donabauer, B ; Reichart, U ; Kolbe, T ; Bogdan, C and Leanderson, Tomas LU , et al. (2003) In Nature Immunology 4(5). p.471-477
Abstract
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... (More)
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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Immunology
volume
4
issue
5
pages
471 - 477
publisher
Nature Publishing Group
external identifiers
  • wos:000182665400015
  • pmid:12679810
  • scopus:0038476601
  • pmid:12679810
ISSN
1529-2908
DOI
10.1038/ni910
language
English
LU publication?
yes
id
2446f80b-bd0b-42dc-9fae-b8b9cee61987 (old id 312464)
date added to LUP
2016-04-01 16:25:29
date last changed
2022-04-15 04:28:36
@article{2446f80b-bd0b-42dc-9fae-b8b9cee61987,
  abstract     = {{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.}},
  author       = {{Karaghiosoff, M and Steinborn, R and Kovarik, P and Kriegshauser, G and Baccarini, M and Donabauer, B and Reichart, U and Kolbe, T and Bogdan, C and Leanderson, Tomas and Levy, D and Decker, T and Muller, M}},
  issn         = {{1529-2908}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{471--477}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Immunology}},
  title        = {{Central role for type I interferons and Tyk2 in lipopolysaccharide-induced endotoxin shock}},
  url          = {{http://dx.doi.org/10.1038/ni910}},
  doi          = {{10.1038/ni910}},
  volume       = {{4}},
  year         = {{2003}},
}