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. 2005 Apr 21;434(7036):1035-40.
doi: 10.1038/nature03547. Epub 2005 Apr 6.

"V体育官网" Spatiotemporal regulation of MyD88-IRF-7 signalling for robust type-I interferon induction

Kenya Honda  1 , Yusuke Ohba, Hideyuki Yanai, Hideo Negishi, Tatsuaki Mizutani, Akinori Takaoka, Choji Taya, Tadatsugu Taniguchi
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Spatiotemporal regulation of MyD88-IRF-7 signalling for robust type-I interferon induction

Kenya Honda et al. Nature. .
Free article

"V体育2025版" Abstract

Robust type-I interferon (IFN-alpha/beta) induction in plasmacytoid dendritic cells, through the activation of Toll-like receptor 9 (TLR9), constitutes a critical aspect of immunity. It is absolutely dependent on the transcription factor IRF-7, which interacts with and is activated by the adaptor MyD88. How plasmacytoid dendritic cells, but not other cell types (such as conventional dendritic cells), are able to activate the MyD88-IRF-7-dependent IFN induction pathway remains unknown. Here we show that the spatiotemporal regulation of MyD88-IRF-7 signalling is critical for a high-level IFN induction in response to TLR9 activation. The IFN-inducing TLR9 ligand, A/D-type CpG oligodeoxynucleotide (CpG-A), is retained for long periods in the endosomal vesicles of plasmacytoid dendritic cells, together with the MyD88-IRF-7 complex VSports手机版. However, in conventional dendritic cells, CpG-A is rapidly transferred to lysosomal vesicles. We further show that conventional dendritic cells can also mount a robust IFN induction if CpG-A is manipulated for endosomal retention using a cationic lipid. This strategy also allows us to demonstrate endosomal activation of the IFN pathway by the otherwise inactive TLR9 ligand B/K-type oligodeoxynucleotide (CpG-B). Thus, our study offers insights into the regulation of TLR9 signalling in space, potentially suggesting a new avenue for therapeutic intervention. .

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