English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

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

MPS-Authors
/persons/resource/persons191059

Freudenberg,  Marina A.
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191214

Merlin,  Thomas
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191140

Kalis,  Christoph
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191064

Galanos,  Chris
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-9616-3
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.