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Published online before print May 18, 2007

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1106707

Received for publication November 29, 2006.
Revised April 30, 2007.
Accepted for publication May 1, 2007.

Article

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 ^*@

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

^@ To whom correspondence should be addressed. E-mail: mkaplan2{at}iupui.edu.

	Abstract

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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