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Beta interferon subtype 1 induction by tumor necrosis factor.

H Jacobsen1, J Mestan, S Mittnacht

  • 1Institute of Virus Research, German Cancer Research Center, Heidelberg, Federal Republic of Germany.

Molecular and Cellular Biology
|July 1, 1989
PubMed
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Tumor necrosis factor (TNF) triggers an antiviral state by inducing interferon-beta 1 (IFN-beta 1) gene transcription in HEp-2 cells. This study demonstrates IFN-beta 1

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Tumor necrosis factor (TNF) induces antiviral states in cells, mimicking interferon (IFN) effects.
  • TNF treatment increases 2',5'-oligoadenylate synthetase activity in HEp-2 cells, an IFN-associated enzyme.
  • Previous studies suggested but did not directly prove IFN-beta 1 induction by TNF.

Purpose of the Study:

  • To directly demonstrate the induction of interferon-beta 1 (IFN-beta 1) by TNF in HEp-2 cells.
  • To investigate the role of IFN-beta 1 as a mediator of TNF's antiviral activity.

Main Methods:

  • Utilized an in vitro DNA amplification protocol for sensitive RNA detection.
  • Analyzed RNA from TNF-treated HEp-2 cells for IFN-beta 1-specific transcripts.
  • Performed Northern blot analysis and nuclear run-on assays to confirm gene expression and transcription.

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Main Results:

  • Demonstrated increased levels of IFN-beta 1-specific transcripts in TNF-treated HEp-2 cells.
  • Observed dose-dependent and kinetic correlation between IFN-beta 1 induction and the antiviral state.
  • Nuclear run-on analysis confirmed enhanced transcriptional activity of the IFN-beta 1 gene.

Conclusions:

  • Interferon-beta 1 (IFN-beta 1) is directly induced by Tumor necrosis factor (TNF) in HEp-2 cells.
  • IFN-beta 1 acts as a key mediator of the antiviral effects elicited by TNF.
  • These findings elucidate a crucial mechanism in TNF-mediated cellular responses.