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Authors
Babdor, JoelDescamps, Delphyne
Adiko, Aimé Cézaire
Tohmé, Mira
Maschalidi, Sophia
Evnouchidou, Irini
Vasconcellos, Luiz Ricardo
De Luca, Mariacristina
Mauvais, Francois-Xavier
Garfa-Traore, Meriem
Brinkmann, Melanie M
Chignard, Michel
Manoury, Bénédicte
Saveanu, Loredana
Issue Date
2017-05
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Show full item recordAbstract
The retention of intracellular Toll-like receptors (TLRs) in the endoplasmic reticulum prevents their activation under basal conditions. TLR9 is activated by sensing ligands in specific endosomal-lysosomal compartments. Here we identified IRAP+ endosomes as major cellular compartments for the early steps of TLR9 activation in dendritic cells (DCs). Both TLR9 and its ligand, the dinucleotide CpG, were present as cargo in IRAP+ endosomes. In the absence of the aminopeptidase IRAP, the trafficking of CpG and TLR9 to lysosomes and signaling via TLR9 were enhanced in DCs and in mice following bacterial infection. IRAP stabilized CpG-containing endosomes by interacting with the actin-nucleation factor FHOD4, which slowed the trafficking of TLR9 toward lysosomes. Thus, endosomal retention of TLR9 via the interaction of IRAP with the actin cytoskeleton is a mechanism that prevents hyper-activation of TLR9 in DCs.Citation
IRAP+ endosomes restrict TLR9 activation and signaling. 2017, 18 (5):509-518 Nat. Immunol.Affiliation
Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.Journal
Nature immunologyDOI
10.1038/ni.3711PubMed ID
28319098Type
ArticleLanguage
enISSN
1529-2916ae974a485f413a2113503eed53cd6c53
10.1038/ni.3711
Scopus Count
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- Creative Commons
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
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