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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

100 Scopus citations

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 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.

Original languageEnglish
Pages (from-to)1927-1932
Number of pages6
JournalScience
Volume311
Issue number5769
DOIs
StatePublished - 31 Mar 2006

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