TLR8 Is a Sensor of RNase T2 Degradation Products.


Journal

Cell
ISSN: 1097-4172
Titre abrégé: Cell
Pays: United States
ID NLM: 0413066

Informations de publication

Date de publication:
27 11 2019
Historique:
received: 10 06 2019
revised: 14 10 2019
accepted: 30 10 2019
entrez: 29 11 2019
pubmed: 30 11 2019
medline: 28 5 2020
Statut: ppublish

Résumé

TLR8 is among the highest-expressed pattern-recognition receptors in the human myeloid compartment, yet its mode of action is poorly understood. TLR8 engages two distinct ligand binding sites to sense RNA degradation products, although it remains unclear how these ligands are formed in cellulo in the context of complex RNA molecule sensing. Here, we identified the lysosomal endoribonuclease RNase T2 as a non-redundant upstream component of TLR8-dependent RNA recognition. RNase T2 activity is required for rendering complex single-stranded, exogenous RNA molecules detectable for TLR8. This is due to RNase T2's preferential cleavage of single-stranded RNA molecules between purine and uridine residues, which critically contributes to the supply of catabolic uridine and the generation of purine-2',3'-cyclophosphate-terminated oligoribonucleotides. Thus-generated molecules constitute agonistic ligands for the first and second binding pocket of TLR8. Together, these results establish the identity and origin of the RNA-derived molecular pattern sensed by TLR8.

Identifiants

pubmed: 31778653
pii: S0092-8674(19)31222-X
doi: 10.1016/j.cell.2019.11.001
pmc: PMC7116005
mid: EMS86706
pii:
doi:

Substances chimiques

Nitrogen Isotopes 0
Nitrogen-15 0
Oligonucleotides 0
Purines 0
Toll-Like Receptor 7 0
Toll-Like Receptor 8 0
RNA 63231-63-0
Endoribonucleases EC 3.1.-
ribonuclease T(2) EC 3.1.27.1
Uridine WHI7HQ7H85

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1264-1275.e13

Subventions

Organisme : European Research Council
ID : 647858
Pays : International
Organisme : Deutsche Forschungsgemeinschaft
Pays : International

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

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Auteurs

Wilhelm Greulich (W)

Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany.

Mirko Wagner (M)

Department of Chemistry, Ludwig-Maximilians-Universität München, Munich, Germany.

Moritz M Gaidt (MM)

Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany; Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA, USA.

Che Stafford (C)

Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany.

Yiming Cheng (Y)

Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany.

Andreas Linder (A)

Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany; Department of Medicine II, University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany.

Thomas Carell (T)

Department of Chemistry, Ludwig-Maximilians-Universität München, Munich, Germany; Center for Integrated Protein Science (CiPSM), Ludwig-Maximilians-Universität München, Munich, Germany. Electronic address: thomas.carell@cup.uni-muenchen.de.

Veit Hornung (V)

Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany; Center for Integrated Protein Science (CiPSM), Ludwig-Maximilians-Universität München, Munich, Germany; Max Planck Institute of Biochemistry, Martinsried, Germany. Electronic address: hornung@genzentrum.lmu.de.

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Classifications MeSH