IL-4-stimulated NF-κB activity is required for Stat6 DNA binding

Vivian T. Thieu, Evelyn T. Nguyen, Brian P. McCarthy, Heather A. Bruns, Reuben Kapur, Cheong Hee Chang, Mark H. Kaplan

Research output: Contribution to journalArticle

22 Scopus citations


IL-4 is a critical cytokine in the regulation of immune responses. In B lymphocytes, IL-4 signaling promotes the Stat6-dependent cell surface expression of several proteins including MHC Class II and CD86. However, the requirement for other transcription factors in IL-4-induced B cell gene expression has not been studied extensively. Here, we show that IL-4 induces NF-κB p100 processing to NF-κB p52 in B cells but not in T cells or macrophages. IL-4 induced NF-κB p52 production requires PI-3K activity and correlates with IκB kinase phosphorylation and TNF receptor-associated factor 3 degradation. Blocking NF-κB activity eliminates IL-4-stimulated gene expression in B cells by reducing IL-4-induced DNA binding but not phosphorylation or nuclear localization of Stat6. These results describe a novel role for NF-κB in IL-4-induced signaling and gene expression.

Original languageEnglish (US)
Pages (from-to)370-379
Number of pages10
JournalJournal of Leukocyte Biology
Issue number2
StatePublished - Aug 1 2007


  • Cytokines
  • Gene regulation
  • p100 processing
  • Transcription factors

ASJC Scopus subject areas

  • Cell Biology

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