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Published online before print May 18, 2007

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(Journal of Leukocyte Biology. 2007;82:370-379.)
© 2007 by Society for Leukocyte Biology

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

Vivian T. Thieu^*,,,, Evelyn T. Nguyen^,, Brian P. McCarthy^*,, Heather A. Bruns^*,, Reuben Kapur^,, Cheong-Hee Chang^*, and Mark H. Kaplan^*,,,,1

Departments of Pediatrics and
^* Microbiology and Immunology,
Wells Center for Pediatric Research and
Walther Oncology Center, Indiana University School of Medicine, and the Walther Cancer Institute, Indianapolis, Indiana, USA

¹ Correspondence: Department of Pediatrics and Microbiology and Immunology, Wells Center for Pediatric Research, 702 Barnhill Drive, RI 2600, Indiana University School of Medicine, Indianapolis, IN 46202, USA. E-mail: mkaplan2{at}iupui.edu

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-B p100 processing to NF-B p52 in B cells but not in T cells or macrophages. IL-4 induced NF-B p52 production requires PI-3K activity and correlates with IB kinase phosphorylation and TNF receptor-associated factor 3 degradation. Blocking NF-B 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-B in IL-4-induced signaling and gene expression.

Key Words: cytokines • gene regulation • transcription factors • p100 processing

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