RIG-I activation is critical for responsiveness to checkpoint blockade.
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
13 09 2019
13 09 2019
Historique:
received:
25
07
2018
revised:
20
05
2019
accepted:
07
08
2019
entrez:
15
9
2019
pubmed:
15
9
2019
medline:
4
6
2020
Statut:
ppublish
Résumé
Achieving durable clinical responses to immune checkpoint inhibitors remains a challenge. Here, we demonstrate that immunotherapy with anti-CTLA-4 and its combination with anti-PD-1 rely on tumor cell-intrinsic activation of the cytosolic RNA receptor RIG-I. Mechanistically, tumor cell-intrinsic RIG-I signaling induced caspase-3-mediated tumor cell death, cross-presentation of tumor-associated antigen by CD103
Identifiants
pubmed: 31519811
pii: 4/39/eaau8943
doi: 10.1126/sciimmunol.aau8943
pii:
doi:
Substances chimiques
Ddx58 protein, mouse
EC 3.6.1.-
DEAD Box Protein 58
EC 3.6.4.13
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.