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Originally published In Press as doi:10.1074/jbc.M910290199 on July 5, 2000

J. Biol. Chem., Vol. 275, Issue 38, 29331-29337, September 22, 2000
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Interleukin-15 Induces Rapid Tyrosine Phosphorylation of STAT6 and the Expression of Interleukin-4 in Mouse Mast Cells*

Akio MasudaDagger , Tetsuya Matsuguchi§, Kenichi YamakiDagger , Tetsuo HayakawaDagger , Masato Kubo||, William J. LaRochelle**, and Yasunobu Yoshikai§

From the Dagger  Second Department of Internal Medicine, § Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya 466-8550, Japan, || Division of Immunobiology, Research Institute for Biological Sciences, Science University of Tokyo, Tokyo 278-0022, Japan, and ** Laboratory of Cellular and Molecular Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892

Interleukin (IL)-4 plays an important role in the differentiation of naive T helper (Th) cells into Th2. Mast cells can produce a significant amount of IL-4 and have been proposed to play a major role in the induction of Th2 responses. Recently, it has been reported that mast cells have a distinct IL-15 receptor system different from that of T or natural killer cells. In the present study, we demonstrated that IL-15 induced IL-4 production from a mouse mast cell line, MC/9, and bone marrow-derived mast cells. IL-4 mRNA expression was increased by IL-15, suggesting that IL-15 promotes IL-4 expression at the transcriptional level. In these mast cells, signal transducer and activator of transcription (STAT) 6 were rapidly tyrosine-phosphorylated in response to IL-15. In MC/9 cells, the expression of a C-terminally truncated dominant negative form of STAT6 significantly suppressed the IL-4 mRNA up-regulation by IL-15, suggesting that STAT6 activation is essential for the IL-15-mediated IL-4 production. Additionally, tyrosine phosphorylation of Tyk2 was rapidly increased by IL-15 treatment in this cell line. Altogether, our results suggest that IL-15 plays an important role in stimulating early IL-4 production in mast cells that may be responsible for the initiation of Th2 response.

* This work was supported by a grant from YASUDA Medical Reserch Foundation, Yakult Bioscience Foundation Grant JSPS-RFTF97L00703, and the Center of Excellence of the Japanese Government.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence and reprint requests should be addressed: Laboratory of Host Defense and Germfree Life, Research Inst. for Disease Mechanism and Control, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. Tel.: (052) 744-2447; Fax: (052) 744-2449; E-mail: tmatsugu@med.nagoya-u.ac.jp.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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