The Journal of Experimental Medicine
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Published 1 July 2002. doi:10.1084/jem.20020026
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© Rockefeller University Press, 0022-1007/2002/7/39/ $5.00
The Journal of Experimental Medicine, Volume 196, Number 1, July 1, 2002 39-49
Induction of NFATc2 Expression by Interleukin 6 Promotes T Helper Type 2 Differentiation

Sean Diehl1, Chi-Wing Chow2, Linda Weiss1, Alois Palmetshofer4, Thomas Twardzik4, Laura Rounds1, Edgar Serfling4, Roger J. Davis2, Juan Anguita3 and Mercedes Rincón1

1 Immunobiology Program, Department of Medicine, Given Medical Building, University of Vermont, Burlington, VT 05405
2 Howard Hughes Medical Institute and Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605
3 Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223
4 Department of Molecular Pathology, Institute of Pathology, University of Würzburg, D-97080 Würzburg, Germany

Address correspondence to Dr. Mercedes Rincón, Given Medical Building D305, University of Vermont, Burlington, VT 05405. Phone: 802-656-0937; Fax: 802-656-3854; E-mail: mrincon{at}zoo.uvm.edu

Interleukin (IL)-6 is produced by professional antigen-presenting cells (APCs) such as B cells, macrophages, and dendritic cells. It has been previously shown that APC-derived IL-6 promotes the differentiation of naive CD4+ T cells into effector T helper type 2 (Th2) cells. Here, we have studied the molecular mechanism for IL-6–mediated Th2 differentiation. During the activation of CD4+ T cells, IL-6 induces the production of IL-4, which promotes the differentiation of these cells into effector Th2 cells. Regulation of IL-4 gene expression by IL-6 is mediated by nuclear factor of activated T cells (NFAT), as inhibition of NFAT prevents IL-6–driven IL-4 production and Th2 differentiation. IL-6 upregulates NFAT transcriptional activity by increasing the levels of NFATc2. The ability of IL-6 to promote Th2 differentiation is impaired in CD4+ T cells that lack NFATc2, demonstrating that NFATc2 is required for regulation of IL-4 gene expression by IL-6. Regulation of NFATc2 expression and NFAT transcriptional activity represents a novel pathway by which IL-6 can modulate gene expression.

Key Words: CD4+ T cells • IL-4 • NFAT • cytokines • gene regulation


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