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J Biol Chem, Vol. 273, Issue 44, 29202-29209, October 30, 1998

STAT6 Is Required for the Anti-inflammatory Activity of Interleukin-4 in Mouse Peritoneal Macrophages

Yoshihiro Ohmori and Thomas A. Hamilton

From the Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195

Interleukin-4 (IL-4) is an anti-inflammatory cytokine which inhibits many inducible macrophage functions. The present study demonstrates that the ability of IL-4 to inhibit interferon gamma (IFNgamma )-dependent gene transcription is dependent upon STAT6. IL-4 suppressed IFNgamma -induced expression of the MIG (monokine induced by IFNgamma ) gene, a C-X-C chemokine, in mouse macrophages. IFNgamma -induced expression of MIG mRNA was abolished in peritoneal macrophages from Stat1-/- mice, and the suppression of MIG mRNA by IL-4 was abolished in macrophages from Stat6-/- mice. Transient transfection assays using a reporter gene containing the MIG gene promoter or the IFNgamma -responsive element (gamma RE) from the MIG gene revealed that the IFNgamma -dependent transcription was suppressed by IL-4, although IL-4 alone had no transactivating function. IFNgamma and IL-4 activated STAT1 and STAT6, respectively, and both proteins were able to bind the gamma RE motif. Furthermore, STAT6 was associated with the co-activator CREB-binding protein in RAW264.7 cells. These observations indicate that STAT6 is necessary for the IL-4-mediated suppression of IFNgamma -induced, STAT1-dependent transcription and suggest that STAT6 may directly suppress the STAT1-dependent transcription by competing with STAT1 for occupancy of the gamma RE motif and/or by competing with limiting quantities of the transcriptional coactivator.


Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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