The Journal of Experimental Medicine
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Published online 2 July 2001. doi:10.1084/jem.194.1.89
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© The Rockefeller University Press, 0022-1007/2001/7/89/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 1, July 2, 2001 89-98

Original Article

Tumor Necrosis Factor Receptor–Associated Factor (Traf)2 Represses the T Helper Cell Type 2 Response through Interaction with Nfat-Interacting Protein (Nip45)

Rebecca Liebersona, Kerri A. Mowena, Kathryn D. McBridea, Veronica Leautauda, Xiankui Zhange, Woong-Kyung Suhd, Lin Wuc, and Laurie H. Glimchera,b

a Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115
b Department of Medicine, Harvard Medical School, Boston, MA 02115
c Arthur D. Little, Cambridge, MA 02140
d Ontario Cancer Institute, Department of Medical Biophysiology and Immunology, Toronto, Ontario M5G 2M9, Canada
e Center for Molecular and Structural Biology, Hollings Oncology Center, Medical University of South Carolina, Charleston, SC 29425
Department of Immunology and Infectious Diseases, Harvard School of Public Health, 651 Huntington Ave., Boston, MA 02115.617-432-0084617-432-0622

lglimche{at}hsph.harvard.edu

Recently we have identified a novel protein NIP45 (nuclear factor of activated T cells [NFAT]-interacting protein) which substantially augments interleukin (IL)-4 gene transcription. The provision of NIP45 together with NFAT and the T helper cell type 2 (Th2)-specific transcription factor c-Maf to cells normally refractory to IL-4 production, such as B cells or Th1 clones, results in substantial IL-4 secretion to levels that approximate those produced by primary Th2 cells. In studies designed to further our understanding of NIP45 activity, we have uncovered a novel facet of IL-4 gene regulation. We present evidence that members of the tumor necrosis factor receptor–associated factor (TRAF) family of proteins, generally known to function as adapter proteins that transduce signals from the tumor necrosis factor receptor superfamily, contribute to the repression of IL-4 gene transcription and that this effect is mediated through their interaction with NIP45.

Key Words: NIP45 • interleukin-4 • cytokines • TRAF2 • transcription

Abbreviations used in this paper: Jnk, c-Jun NH2-terminal kinase; NFAT, nuclear factor of activated T cells; NIP45, NFAT-interacting protein.

© 2001 The Rockefeller University Press


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