Stimulation-specific contribution of p38 and JNK to IFN-beta gene expression in human macrophages

Reimer, Thornik; Schweizer, Matthias; Jungi, Thomas W (2007). Stimulation-specific contribution of p38 and JNK to IFN-beta gene expression in human macrophages. Journal of interferon & cytokine research, 27(9), pp. 751-5. New York, N.Y.: Mary Ann Liebert 10.1089/jir.2007.0024

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Induction of interferon-beta (IFN-beta) gene expression is a tightly regulated process, and a plethora of studies identified the signal transduction pathway TANK-binding kinase-1 (TBK-1)/IFN regulatory factor-3 (IRF-3) as essential to the induction of IFN-beta gene expression. Data regarding the role of p38 and JNK are rare, however. We investigated the contribution of these kinases to IFN-beta expression in human macrophages treated with poly(I:C), lipopolysaccharide (LPS), Sendai virus, or vesicular stomatitis virus (VSV). We found that all the stimuli induced IFN-beta mRNA, albeit to a different extent. Whereas LPS and VSV induced the phosphorylation of p38 and JNK, neither poly(I:C) nor Sendai virus led to the detection of phosphospecific signals. When inhibiting p38, a VSV-triggered IFN-beta mRNA response was inhibited, whereas inhibiting JNK suppressed an LPS-triggered response, but only when macrophages were primed with IFN-gamma. Neither poly(I:C)-induced nor Sendai virus-induced IFN-beta mRNA expression was affected when p38 and JNK were inhibited. Collectively, the data show that the contribution of p38 and JNK to the expression of IFN-beta occurs in a stimulation-specific manner in human macrophages.

Item Type:

Journal Article (Original Article)


05 Veterinary Medicine > Department of Infectious Diseases and Pathobiology (DIP) > Institute of Virology and Immunology

UniBE Contributor:

Reimer, Thornik, Schweizer, Matthias, Jungi, Thomas




Mary Ann Liebert




Factscience Import

Date Deposited:

04 Oct 2013 14:54

Last Modified:

05 Dec 2022 14:16

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URI: (FactScience: 37859)

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