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Gewählte Publikation:

Schneider, A; Reichart, U; Gerner, W; Kolbe, T; Saalmüller, A; Müller, M.
(2008): Selective contribution of Tyk2 to cell activation by lipopolysaccharide.
FEBS Lett. 2008; 582(25-26):3681-3686 FullText FullText_BOKU

Tyk2 deficient mice show a markedly reduced susceptibility to lipopolysaccharide (LPS) induced shock and a partial impairment of IL-12 and interferon (IFN) signals. To examine the underlying mechanisms, we analysed the activation of peritoneal macrophages (PM phi s) and spleen cells after LPS challenge. In PMUs and spleen cells the contribution of Tyk2 to the induction of the T-cell co-stimulatory molecules CD86, CD40 and MHC II was small or insignificant. By contrast, induced expression of the early activation marker CD69 on PMUs and splenic cell populations required type I interferons (IFN-I) and Tyk2. The data suggest a selective contribution of Tyk2 to the activation of inflammation-relevant cell types by LPS. (c) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
Autor*innen der BOKU Wien:
Kolbe Thomas
BOKU Gendermonitor:

Find related publications in this database (using NML MeSH Indexing)
Animals -
Antigens, CD - immunology
Antigens, CD86 - immunology
Antigens, Differentiation, T-Lymphocyte - immunology
Interferon Type I - immunology
Interferons - immunology
Interleukin-12 - immunology
Lipopolysaccharides - immunology
Lymphocyte Activation - genetics
Macrophage Activation - genetics
Macrophages, Peritoneal - enzymology
Male -
Mice -
Mice, Mutant Strains -
Receptor, Interferon alpha-beta - immunology
Spleen - cytology
T-Lymphocytes - enzymology
TYK2 Kinase - genetics
Up-Regulation -

Find related publications in this database (Keywords)
Co-stimulatory molecule
Interferon (IFN)
Janus kinase (Jak)

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