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Rel induces interferon regulatory factor 4 (IRF-4) expression in lymphocytes: modulation of interferon-regulated gene

R J Grumont1, S Gerondakis

  • 1Walter and Eliza Hall Institute of Medical Research, The Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.

The Journal of Experimental Medicine
|April 19, 2000
PubMed

Insights

The Rel transcription factor controls interferon regulatory factor 4 (IRF-4) expression in lymphocytes. This finding reveals a new way Rel/nuclear factor kappaB represses interferon-regulated genes, impacting cell proliferation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • The Rel transcription factor is crucial for lymphocyte gene expression, influencing proliferation, survival, and differentiation.
  • Interferon (IFN) regulatory factor 4 (IRF-4) is a lymphoid-specific transcription factor within the IFN family.

Purpose of the Study:

  • To investigate the relationship between Rel transcription factor and IRF-4 expression in lymphocytes.
  • To elucidate the role of IRF-4 in mediating the effects of IFNs on lymphocyte proliferation.
  • To understand the cross-regulation between Rel/nuclear factor kappaB and IFN signaling pathways.

Main Methods:

  • Analysis of mitogen-induced IRF-4 expression in lymphocytes.
  • Comparison of IFN sensitivity in wild-type and c-rel(-/-) B cells.
  • Enforced expression of an IRF-4 transgene in c-rel(-/-) B cells.

Main Results:

  • Mitogen-induced IRF-4 expression is dependent on the Rel transcription factor.
  • Absence of IRF-4 in c-rel(-/-) B cells leads to increased sensitivity to IFN's antiproliferative effects.
  • Restoration of IRF-4 expression in c-rel(-/-) B cells normalized IFN-modulated proliferation.

Conclusions:

  • IRF-4 acts as a repressor of IFN-induced gene expression.
  • Rel/nuclear factor kappaB represses IFN-regulated genes in a cell type-specific manner through IRF-4.
  • This cross-regulation highlights a novel mechanism for controlling lymphocyte gene expression and response to interferons.

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