CD40 employs p38 MAP kinase in IgE isotype switching

K. Brady, S. Fitzgerald, Sigurdur Ingvarsson, Carl Borrebaeck, P. N. Moynagh

Research output: Contribution to journalArticlepeer-review

Abstract

IgE switching requires the prior induction of CE germline transcripts which is mediated by the concerted binding of STAT-6 and NF kappaB to the CE promoter. These transcription factors are regulated by IL-4 and CD40, respectively. However the latter can effect other signaling pathways and the present study explores the role of p38 MAPK in induction of CE germline transcripts. CD40 and IL-4, both alone and in synergy, were initially shown to activate the CE promoter in a B cell lymphoma cell line. Under the same conditions CD40 caused activation of p38 MAPK, whereas IL-4 was ineffective. The p38 MAPK inhibitor, SB203580, and a dominant negative form of p38 MAPK decreased the CD40 activation of the CE promoter by reducing the ability of CD40 to increase the transactivation potential of NF kappaB. This study suggests that p38 MAPK is crucially important in mediating CD40 activation of NFKB which acts to induce CE germline transcripts, ultimately facilitating IgE switching. (C) 2001 Academic Press.
Original languageEnglish
Pages (from-to)276-281
JournalBiochemical and Biophysical Research Communications
Volume289
Issue number1
DOIs
Publication statusPublished - 2001

Subject classification (UKÄ)

  • Biological Sciences

Free keywords

  • CD40
  • IgE
  • isotype switching
  • allergy
  • p38 MAP kinase
  • NF kappa B
  • ACTIVATED PROTEIN-KINASE
  • TUMOR-NECROSIS-FACTOR
  • CROSS-LINKING CD40
  • FACTOR-KAPPA-B
  • GERMLINE PROMOTER
  • CELLS
  • TRANSCRIPTION
  • INTERLEUKIN-4
  • EXPRESSION
  • MICE

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