| First Author | Suzuki N | Year | 2006 |
| Journal | Science | Volume | 311 |
| Issue | 5769 | Pages | 1927-32 |
| PubMed ID | 16574867 | Mgi Jnum | J:107198 |
| Mgi Id | MGI:3620400 | Doi | 10.1126/science.1124256 |
| Citation | Suzuki N, et al. (2006) A critical role for the innate immune signaling molecule IRAK-4 in T cell activation. Science 311(5769):1927-32 |
| abstractText | 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. |
