A critical role for the innate immune signaling molecule IRAK-4 in T cell activation |
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Authors: | Suzuki Nobutaka Suzuki Shinobu Millar Douglas G Unno Midori Hara Hiromitsu Calzascia Thomas Yamasaki Sho Yokosuka Tadashi Chen Nien-Jung Elford Alisha R Suzuki Jun-Ichiro Takeuchi Arata Mirtsos Christine Bouchard Denis Ohashi Pamela S Yeh Wen-Chen Saito Takashi |
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Affiliation: | Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama City, Kanagawa 230-0045, Japan. |
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Abstract: | 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 C activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor kappaB. 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. |
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