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  Absence of TRIF Signaling in Lipopolysaccharide-Stimulated Murine Mast Cells

Keck, S., Müller, I., Fejer, G., Savic, I., Tchaptchet, S., Nielsen, P. J., et al. (2011). Absence of TRIF Signaling in Lipopolysaccharide-Stimulated Murine Mast Cells. The Journal of Immunology, 186, 5478-5488.

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 Creators:
Keck, Simone1, Author           
Müller, Ines2, Author           
Fejer, György2, Author           
Savic, Iva3, Author
Tchaptchet, Sandrine2, Author           
Nielsen, Peter J.4, Author           
Galanos, Chris1, Author           
Huber, Michael4, Author           
Freudenberg, Marina A.2, Author           
Affiliations:
1Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              
2Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
3Max Planck Society, ou_persistent13              
4Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243645              

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 Abstract: In macrophages, two signaling pathways, dependent on MyD88 or TIR domain-containing adaptor-inducing IFN-β (TRIF) signaling, emanate from the LPS receptor TLR4/MD-2. In this study, we show that in murine bone marrow-derived mast cells (BMMCs), only the MyD88-dependent pathway is activated by LPS. The TRIF signaling branch leading both to NF-κB activation and enhanced proinflammatory cytokine production, as well as to IRF3 activation and subsequent IFN-β production, is absent in LPS-stimulated BMMCs. IRF3 activation is also absent in peritoneal mast cells from LPS-injected mice. We observed strongly diminished TRAM expression in BMMCs, but overexpression of TRAM only moderately enhanced IL-6 and did not boost IFN-β responses to LPS in these cells. A combination of very low levels of TRAM and TLR4/MD-2 with the known absence of membrane-bound CD14 are expected to contribute to the defective TRIF signaling in mast cells. We also show that, unlike in macrophages, in BMMCs the TRIF-dependent and -independent IFN-αβ responses to other recognized IFN inducers (dsRNA, adenovirus, and B-DNA) are absent. These results show how the response to the same microbial ligand using the same receptor can be regulated in different cell types of the innate immune system.

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Language(s): eng - English
 Dates: 2011
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: eDoc: 577445
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Title: The Journal of Immunology
  Alternative Title : J. Immunol.
Source Genre: Journal
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Pages: - Volume / Issue: 186 Sequence Number: - Start / End Page: 5478 - 5488 Identifier: -