Interleukin-15 Prevents Mouse Mast Cell Apoptosis through STAT6-mediated Bcl-xL Expression

Akio Masuda, Tetsuya Matsuguchi, Kenichi Yamaki, Tetsuo Hayakawa, Yasunobu Yoshikai

    研究成果: ジャーナルへの寄稿記事

    64 引用 (Scopus)

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    Interleukin (IL)-15 is a member of the cytokine family with T and natural killer (NK) cell growth-promoting activity. In mast cells, however, IL-15 uses a distinct receptor system different from that used in T and NK cells. We recently reported that IL-15 induces STAT6 activation and IL-4 production in a mouse mast cell line (MC/9) and bone marrow-derived mast cells. In the present study, we have demonstrated that IL-15 prevents MC/9 and bone marrow-derived mast cell apoptosis induced by factor withdrawal or anti-Fas antibody treatment. IL-15 increased mRNA and protein levels of an anti-apoptotic protein (Bcl-xL) in these cells, whereas bcl-2 mRNA remained unchanged. In addition, the transcriptional activity of the bcl-xL promoter was increased by IL-15 in MC/9 cells. In an electrophoretic mobility shift assay, IL-15 induced STAT6 binding to the STAT recognition site in the bcl-x L gene promoter. Furthermore, the expression of a dominant-negative form of STAT6 abrogated the effects of IL-15 on both bcl-xL mRNA up-regulation and prevention of apoptosis in mast cells. Altogether, our results suggest that IL-15 plays an important role in maintaining the number of mast cells through Bcl-xL expression mediated by STAT6.

    元の言語英語
    ページ(範囲)26107-26113
    ページ数7
    ジャーナルJournal of Biological Chemistry
    276
    発行部数28
    DOI
    出版物ステータス出版済み - 7 13 2001

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    All Science Journal Classification (ASJC) codes

    • Biochemistry

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