| First Author | Hoshino K | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 7 | Pages | 3341-5 |
| PubMed ID | 20200270 | Mgi Jnum | J:160080 |
| Mgi Id | MGI:4453397 | Doi | 10.4049/jimmunol.0901648 |
| Citation | Hoshino K, et al. (2010) Critical role of IkappaB Kinase alpha in TLR7/9-induced type I IFN production by conventional dendritic cells. J Immunol 184(7):3341-5 |
| abstractText | A plasmacytoid dendritic cell (DC) can produce large amounts of type I IFNs after sensing nucleic acids through TLR7 and TLR9. IkappaB kinase alpha (IKKalpha) is critically involved in this type I IFN production through its interaction with IFN regulatory factor-7. In response to TLR7/9 signaling, conventional DCs can also produce IFN-beta but not IFN-alpha in a type I IFN-independent manner. In this study, we showed that IKKalpha was required for production of IFN-beta, but not of proinflammatory cytokines, by TLR7/9-stimulated conventional DCs. Importantly, IKKalpha was dispensable for IFN-beta gene upregulation by TLR4 signaling. Biochemical analyses indicated that IKKalpha exerted its effects through its interaction with IFN regulatory factor-1. Furthermore, IKKalpha was involved in TLR9-induced type I IFN-independent IFN-beta production in vivo. Our results show that IKKalpha is a unique molecule involved in TLR7/9-MyD88-dependent type I IFN production through DC subset-specific mechanisms. |
