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