Journalartikel
Autorenliste: Stockinger, S; Materna, T; Stoiber, D; Bayr, L; Steinborn, R; Kolbe, T; Unger, H; Chakraborty, T; Levy, DE; Müller, M; Decker, T
Jahr der Veröffentlichung: 2002
Seiten: 6522-6529
Zeitschrift: The Journal of Immunology
Bandnummer: 169
Heftnummer: 11
ISSN: 0022-1767
DOI Link: https://doi.org/10.4049/jimmunol.169.11.6522
Verlag: American Association of Immunologists
Abstract:
Type I IFNs (IFN-alpha/beta) modulate innate immune responses. Here we show activation of transcription factor IFN regulatory factor 3, the synthesis of large amounts of IFN-beta mRNA, and type I IFN signal transduction in macrophages infected with Listeria monocytogenes. Expression of the bacterial virulence protein listeriolysin O was necessary, but not sufficient, for efficient IFN-beta production. Signaling through a pathway involving the type I IFN receptor and Stat1 sensitized macrophages to L. monocytogenes-induced cell death in a manner not requiring inducible NO synthase (nitric oxide synthase 2) or protein kinase R, potential effectors of type I IFN action during microbial infections. The data stress the importance of type I IFN for the course of infections with intracellular bacteria and suggest that factors other than listeriolysin O contribute to macrophage death during Listeria infection.
Zitierstile
Harvard-Zitierstil: Stockinger, S., Materna, T., Stoiber, D., Bayr, L., Steinborn, R., Kolbe, T., et al. (2002) Production of type IIFN sensitizes macrophages to cell death induced by Listeria monocytogenes, The Journal of Immunology, 169(11), pp. 6522-6529. https://doi.org/10.4049/jimmunol.169.11.6522
APA-Zitierstil: Stockinger, S., Materna, T., Stoiber, D., Bayr, L., Steinborn, R., Kolbe, T., Unger, H., Chakraborty, T., Levy, D., Müller, M., & Decker, T. (2002). Production of type IIFN sensitizes macrophages to cell death induced by Listeria monocytogenes. The Journal of Immunology. 169(11), 6522-6529. https://doi.org/10.4049/jimmunol.169.11.6522
Schlagwörter
BACILLUS-SUBTILIS; MURINE MACROPHAGES; NITRIC-OXIDE SYNTHASE; VIRUS-INDUCED APOPTOSIS