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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

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons191059

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

http://pubman.mpdl.mpg.de/cone/persons/resource/persons191214

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

http://pubman.mpdl.mpg.de/cone/persons/resource/persons191140

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

http://pubman.mpdl.mpg.de/cone/persons/resource/persons191064

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

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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: http://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.