The Unfolded Protein Response Mediator PERK Governs Myeloid Cell-Driven Immunosuppression in Tumors through Inhibition of STING Signaling.
Animals
CD8-Positive T-Lymphocytes
/ immunology
Carcinoma, Lewis Lung
/ genetics
Carcinoma, Ovarian Epithelial
/ genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Immunosuppression Therapy
Interferon-alpha
/ genetics
Interferon-beta
/ genetics
Male
Melanoma, Experimental
/ genetics
Membrane Proteins
/ genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondria
/ immunology
Myeloid-Derived Suppressor Cells
/ immunology
NF-E2-Related Factor 2
/ genetics
Receptors, Interferon
/ genetics
Signal Transduction
Skin Neoplasms
/ genetics
Unfolded Protein Response
/ immunology
eIF-2 Kinase
/ deficiency
ER stress
MDSCs
NRF2
PERK
STING
tumor immunity
type I IFN
unfolded protein responses
Journal
Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918
Informations de publication
Date de publication:
14 04 2020
14 04 2020
Historique:
received:
14
05
2019
revised:
14
01
2020
accepted:
12
03
2020
entrez:
16
4
2020
pubmed:
16
4
2020
medline:
5
11
2020
Statut:
ppublish
Résumé
The primary mechanisms supporting immunoregulatory polarization of myeloid cells upon infiltration into tumors remain largely unexplored. Elucidation of these signals could enable better strategies to restore protective anti-tumor immunity. Here, we investigated the role of the intrinsic activation of the PKR-like endoplasmic reticulum (ER) kinase (PERK) in the immunoinhibitory actions of tumor-associated myeloid-derived suppressor cells (tumor-MDSCs). PERK signaling increased in tumor-MDSCs, and its deletion transformed MDSCs into myeloid cells that activated CD8
Identifiants
pubmed: 32294407
pii: S1074-7613(20)30117-5
doi: 10.1016/j.immuni.2020.03.004
pmc: PMC7207019
mid: NIHMS1579139
pii:
doi:
Substances chimiques
Interferon-alpha
0
Membrane Proteins
0
NF-E2-Related Factor 2
0
Nfe2l2 protein, mouse
0
Receptors, Interferon
0
Sting1 protein, mouse
0
Interferon-beta
77238-31-4
PERK kinase
EC 2.7.11.1
eIF-2 Kinase
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
668-682.e7Subventions
Organisme : NCI NIH HHS
ID : R01 CA233512
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA211229
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA009140
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA103320
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA076292
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA157664
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA178687
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA124515
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA184185
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Interests The authors declare no competing interests.
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