The interaction between IKKα and LC3 promotes type I interferon production through the TLR9-containing LAPosome.

ABSTRACT: Toll-like receptor 9 (TLR9) recognizes DNA in endosomes and activates distinct signaling pathways to stimulate the production of proinflammatory cytokines and type I interferons (IFNs). The assembly of signaling platforms on microtubule-associated proteins 1A/1B-light chain 3 (LC3)-decorated endosomal vesicles is required to transduce TLR9 signals that stimulate the production of IFN but not interleukin-12 p40 (IL-12p40). LC3-associated phagocytosis (LAP), a form of noncanonical autophagy, is critical for the activation of interferon regulatory factor 7 (IRF7) and for IFN synthesis. We showed that after the stimulation of TLR9 by CpG oligonucleotides, the autophagy protein LC3 and the kinase IKKα were recruited to endosomes that contained TLR9. The recruitment of IKKα and LC3 to such signa

SUBMITTER: Hayashi K 

PROVIDER: S-EPMC6462218 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature