Abstract

A plasmacytoid dendritic cell (DC) can produce large amounts of type I IFNs after sensing nucleic acids through TLR7 and TLR9. IκB kinase α (IKKα) 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-β but not IFN-α in a type I IFN-independent manner. In this study, we showed that IKKα was required for production of IFN-β, but not of proinflammatory cytokines, by TLR7/9-stimulated conventional DCs. Importantly, IKKα was dispensable for IFN-β gene upregulation by TLR4 signaling. Biochemical analyses indicated that IKKα exerted its effects through its interaction with IFN regulatory factor-1. Furthermore, IKKα was involved in TLR9-induced type I IFN-independent IFN-β production in vivo. Our results show that IKKα is a unique molecule involved in TLR7/9-MyD88–dependent type I IFN production through DC subset-specific mechanisms.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://dbpia.nl.go.kr/pages/standard-publication-reuse-rights)
You do not currently have access to this article.