Role of activator protein 1, nuclear factor-kappaB, and nuclear factor of activated T cells in IgE receptor-mediated cytokine expression in mature human mast cells

J Allergy Clin Immunol. 2003 May;111(5):1062-8. doi: 10.1067/mai.2003.1342.

Abstract

Background: On activation by cross-linking the high-affinity IgE receptor (FcepsilonRI), expression of TNF-alpha, IL-3, IL-5, and IL-13 is induced in human intestinal mast cells.

Objective: We sought to examine, for the first time, FcepsilonRI signaling in mature human mast cells.

Methods: Mast cells were isolated from intestinal tissue and cultured in the presence of stem cell factor. The cells were treated with specific inhibitors before stimulation by means of FcepsilonRI cross-linking. Cytokine mRNA expression was analyzed by means of RT-PCR, and activation of signaling molecules was determined by means of immunocytochemistry, RT-PCR, Western blotting, and protein kinase C (PKC) assay.

Results: We found that nuclear factor-kappaB (NF-kappaB), as well as c-Fos and c-Jun, the components of activator protein 1 (AP-1), are activated after FcepsilonRI cross-linking in human intestinal mast cells. Treatment of the cells with specific inhibitors revealed an involvement of NF-kappaB and nuclear factor of activated T cells, as well as the necessity of extracellular signal-regulated kinase 1/2 (ERK-1/2), PKC, and AP-1 for the induced cytokine gene expression. Consistently, we found that activation of c-Fos corresponds with the induced cytokine gene expression and that ERK-1/2, an activator of c-Fos, was activated in response to FcepsilonRI cross-linking.

Conclusion: Our data on human mast cells show that the activity of ERK-1/2, PKC, and subsequent activation of AP-1 are necessary for the FcepsilonRI-mediated cytokine expression. Nuclear factor of activated T cells and NF-kappaB seem to be necessary for the induction of TNF-alpha, IL-3, and IL-13 but are less important for the transcription of IL-5.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cytokines / genetics*
  • DNA-Binding Proteins / physiology*
  • Genes, fos
  • Genes, jun
  • Humans
  • Interleukin-13 / genetics
  • Interleukin-3 / genetics
  • Interleukin-5 / genetics
  • Mast Cells / immunology*
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / physiology*
  • NFATC Transcription Factors
  • Nuclear Proteins*
  • Protein Kinase C / physiology
  • RNA, Messenger / analysis
  • Receptors, IgE / physiology*
  • Signal Transduction
  • Transcription Factor AP-1 / physiology*
  • Transcription Factors / physiology*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Cytokines
  • DNA-Binding Proteins
  • Interleukin-13
  • Interleukin-3
  • Interleukin-5
  • NF-kappa B
  • NFATC Transcription Factors
  • Nuclear Proteins
  • RNA, Messenger
  • Receptors, IgE
  • Transcription Factor AP-1
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Protein Kinase C
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases