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

نویسندگان

  • 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
چکیده

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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عنوان ژورنال:
  • Science

دوره 311 5769  شماره 

صفحات  -

تاریخ انتشار 2006