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Interferon regulatory factor 4 (IRF4) interacts with NFATc2 to modulate interleukin 4 gene expression

Academic Article
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Overview

authors

  • Rengarajan, J.
  • Mowen, Kerri
  • McBride, K. D.
  • Smith, E. D.
  • Singh, H.
  • Glimcher, L. H.

publication date

  • April 2002

journal

  • Journal of Experimental Medicine  Journal

abstract

  • Proteins of the nuclear factor of activated T cells (NFAT) family of transcription factors are critical for lymphocyte activation in the immune system. In particular, NFATs are important regulators of inducible IL-4 gene expression. Interferon regulatory factor 4 (IRF4) is an immune system-restricted interferon regulatory factor that is required for lymphocyte activation, but its molecular functions in the T lineage remain to be elucidated. We demonstrate that IRF4 potently synergizes with NFATc2 to specifically enhance NFATc2-driven transcriptional activation of the IL-4 promoter. This function is dependent on the physical interaction of IRF4 with NFATc2. IRF4 synergizes with NFATc2 and the IL-4-inducing transcription factor, c-maf, to augment IL-4 promoter activity as well as to elicit significant levels of endogenous IL-4 production. Furthermore, na?ve T helper cells from mice lacking IRF4 are compromised severely for the production of IL-4 and other Th2 cytokines. The identification of IRF4 as a partner for NFATc2 in IL-4 gene regulation provides an important molecular function for IRF4 in T helper cell differentiation.
  • Proteins of the nuclear factor of activated T cells (NFAT) family of transcription factors are critical for lymphocyte activation in the immune system. In particular, NFATs are important regulators of inducible IL-4 gene expression. Interferon regulatory factor 4 (IRF4) is an immune system-restricted interferon regulatory factor that is required for lymphocyte activation, but its molecular functions in the T lineage remain to be elucidated. We demonstrate that IRF4 potently synergizes with NFATc2 to specifically enhance NFATc2-driven transcriptional activation of the IL-4 promoter. This function is dependent on the physical interaction of IRF4 with NFATc2. IRF4 synergizes with NFATc2 and the IL-4-inducing transcription factor, c-maf, to augment IL-4 promoter activity as well as to elicit significant levels of endogenous IL-4 production. Furthermore, naïve T helper cells from mice lacking IRF4 are compromised severely for the production of IL-4 and other Th2 cytokines. The identification of IRF4 as a partner for NFATc2 in IL-4 gene regulation provides an important molecular function for IRF4 in T helper cell differentiation.

subject areas

  • Animals
  • Binding Sites
  • Cell Differentiation
  • Cell Line, Transformed
  • DNA-Binding Proteins
  • Humans
  • Interferon Regulatory Factors
  • Interleukin-4
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • NFATC Transcription Factors
  • Nuclear Proteins
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-maf
  • Th2 Cells
  • Transcription Factors
  • Transcriptional Activation
  • Tumor Cells, Cultured
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Research

keywords

  • IL-4
  • IRF4
  • NFAT
  • interaction
  • transcriptional regulation
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Identity

PubMed Central ID

  • PMC2193700

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.20011128

PubMed ID

  • 11956291
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Additional Document Info

start page

  • 1003

end page

  • 1012

volume

  • 195

issue

  • 8

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