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IL‐4‐stimulated NF‐κB activity is required for Stat6 DNA binding
Author(s) -
Thieu Vivian T.,
Nguyen Evelyn T.,
McCarthy Brian P.,
Bruns Heather A.,
Kapur Reuben,
Chang CheongHee,
Kaplan Mark H.
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1106707
Subject(s) - biology , nf κb , dna , microbiology and biotechnology , nfkb1 , stat6 , signal transduction , cancer research , transcription factor , immune system , genetics , interleukin 4 , gene
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.