A critical role for the innate immune signaling molecule IRAK-4 in T cell activation

Nobutaka Suzuki, Shinobu Suzuki, Douglas G. Millar, Midori Unno, Hiromitsu Hara, Thomas Calzascia, Sho Yamasaki, Tadashi Yokosuka, Nien Jung Chen, Alisha R. Elford, Jun Ichiro Suzuki, Arata Takeuchi, Christine Mirtsos, Denis Bouchard, Pamela S. Ohashi, Wen Chen Yeh, Takashi Saito

    研究成果: Contribution to journalArticle査読

    88 被引用数 (Scopus)

    抄録

    IRAK-4 is a protein kinase that is pivotal in mediating signals for innate immune responses. Here, we report that IRAK-4 signaling is also essential for eliciting adaptive immune responses. Thus, in the absence of IRAK-4, in vivo T cell responses were significantly impaired. Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase Cθ activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor κB. Our findings suggest that T cells use this critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems.

    本文言語英語
    ページ(範囲)1927-1932
    ページ数6
    ジャーナルScience
    311
    5769
    DOI
    出版ステータス出版済み - 3 31 2006

    All Science Journal Classification (ASJC) codes

    • General

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