The Journal of Experimental Medicine
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Published online 8 April 2002 doi:10.1084/jem.20011128
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© Rockefeller University Press, 0022-1007/2002/4/1003/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 8, April 15, 2002 1003-1012
Interferon Regulatory Factor 4 (IRF4) Interacts with NFATc2 to Modulate Interleukin 4 Gene Expression

Jyothi Rengarajan1, Kerri A. Mowen1, Kathryn D. McBride1, Erica D. Smith3, Harinder Singh3 and Laurie H. Glimcher1,2

1 Department of Immunology and Infectious Disease, Harvard School of Public Health, Boston, MA 02115
2 Department of Medicine, Harvard Medical School, Boston, MA 02115
3 Howard Hughes Medical Institute, The University of Chicago, Chicago, IL 60637

Address correspondence to L.H. Glimcher, Department of Immunology and Infectious Disease, Harvard School of Public Health, Harvard Medical School, Boston, MA 02115. Phone: (617) 432-0622; Fax: (617) 432-0084; E-mail: lglimche{at}hsph.harvard.edu

Proteins of the nuclear factor of activated T cells (NFAT) family of transcription factors are critical for lymphocyte activation in the immune system. In particular, NFATs are important regulators of inducible IL-4 gene expression. Interferon regulatory factor 4 (IRF4) is an immune system–restricted interferon regulatory factor that is required for lymphocyte activation, but its molecular functions in the T lineage remain to be elucidated. We demonstrate that IRF4 potently synergizes with NFATc2 to specifically enhance NFATc2-driven transcriptional activation of the IL-4 promoter. This function is dependent on the physical interaction of IRF4 with NFATc2. IRF4 synergizes with NFATc2 and the IL-4–inducing transcription factor, c-maf, to augment IL-4 promoter activity as well as to elicit significant levels of endogenous IL-4 production. Furthermore, naïve T helper cells from mice lacking IRF4 are compromised severely for the production of IL-4 and other Th2 cytokines. The identification of IRF4 as a partner for NFATc2 in IL-4 gene regulation provides an important molecular function for IRF4 in T helper cell differentiation.

Key Words: IRF4 • NFAT • IL-4 • transcriptional regulation • interaction


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