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J Biol Chem, Vol. 273, Issue 44, 29202-29209, October 30, 1998
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
STAT6 Is Required for the Anti-inflammatory Activity of
Interleukin-4 in Mouse Peritoneal Macrophages
(IFN)-dependent gene transcription is
dependent upon STAT6. IL-4 suppressed IFN-induced expression of the
MIG (monokine induced by IFN)
gene, a C-X-C chemokine, in mouse macrophages. IFN-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 IFN-responsive element (RE) from the MIG
gene revealed that the IFN-dependent transcription was
suppressed by IL-4, although IL-4 alone had no transactivating
function. IFN and IL-4 activated STAT1 and STAT6, respectively, and
both proteins were able to bind the 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 IFN-induced,
STAT1-dependent transcription and suggest that STAT6 may
directly suppress the STAT1-dependent transcription by
competing with STAT1 for occupancy of the 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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