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  Cutting Edge: A Murine, IL-12-Independent Pathway of IFN-γ Induction by Gram-Negative: Bacteria Based on STAT4 Activation by Type I IFN and IL-18 Signaling¹

Freudenberg, M. A., Merlin, T., Kalis, C., Chvatchko, Y., Stübig, H., & Galanos, C. (2002). Cutting Edge: A Murine, IL-12-Independent Pathway of IFN-γ Induction by Gram-Negative: Bacteria Based on STAT4 Activation by Type I IFN and IL-18 Signaling¹. The Journal of Immunology, 169(4), 1665-1668.

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 Creators:
Freudenberg, Marina A.1, Author           
Merlin, Thomas2, Author           
Kalis, Christoph2, Author           
Chvatchko, Yolande, Author
Stübig, Hella, Author
Galanos, Chris2, Author           
Affiliations:
1Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
2Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              

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 Abstract: IFN-αβ is a potent immunoregulatory cytokine involved in the defense against viral and bacterial infections. In this study, we describe an as yet undefined IFN-αβ-dependent pathway of IFN-γ induction in mice. This pathway is based on a synergism of IFN-αβ and IL-18, and is independent of IL-12 signaling yet dependent on STAT4. In contradiction to current dogma, we show further that IFN-αβ alone induces tyrosine phosphorylation of STAT4 in murine splenocytes of different mouse strains. This pathway participates in the induction of IFN-γ by Gram-negative bacteria and is therefore expected to play a role whenever IFN-α or IFN-β and IL-18 are produced concomitantly during bacterial, viral, or other infections.

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Language(s): eng - English
 Dates: 2002-08-15
 Publication Status: Issued
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 18549
ISI: 000177365800001
 Degree: -

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Title: The Journal of Immunology
  Alternative Title : J. Immunol.
Source Genre: Journal
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Pages: - Volume / Issue: 169 (4) Sequence Number: - Start / End Page: 1665 - 1668 Identifier: ISSN: 0022-1767