Interleukin-10 receptor signaling promotes the maintenance of a PD-1
Animals
CD8-Positive T-Lymphocytes
/ immunology
Cell Line, Tumor
Cells, Cultured
Cellular Microenvironment
Hepatocyte Nuclear Factor 1-alpha
/ metabolism
Humans
Immunity
Immunotherapy
/ methods
Leukemia, Lymphocytic, Chronic, B-Cell
/ immunology
Mice
Mice, Inbred C57BL
NFATC Transcription Factors
/ metabolism
Programmed Cell Death 1 Receptor
/ metabolism
Receptors, Interleukin-10
/ genetics
STAT3 Transcription Factor
/ genetics
Signal Transduction
T-Lymphocyte Subsets
/ immunology
Transcription Factor AP-1
/ metabolism
CD8(+) T cells
CLL
IL-10
IL-10R
NFAT
PD-1 heterogeneity
STAT3
T cell exhaustion
TCF-1
tumor microenvironment
Journal
Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918
Informations de publication
Date de publication:
14 12 2021
14 12 2021
Historique:
received:
09
01
2021
revised:
26
03
2021
accepted:
09
11
2021
pubmed:
9
12
2021
medline:
19
2
2022
entrez:
8
12
2021
Statut:
ppublish
Résumé
T cell exhaustion limits anti-tumor immunity and responses to immunotherapy. Here, we explored the microenvironmental signals regulating T cell exhaustion using a model of chronic lymphocytic leukemia (CLL). Single-cell analyses identified a subset of PD-1
Identifiants
pubmed: 34879221
pii: S1074-7613(21)00495-7
doi: 10.1016/j.immuni.2021.11.004
pii:
doi:
Substances chimiques
Hepatocyte Nuclear Factor 1-alpha
0
Hnf1a protein, mouse
0
NFATC Transcription Factors
0
Programmed Cell Death 1 Receptor
0
Receptors, Interleukin-10
0
STAT3 Transcription Factor
0
Transcription Factor AP-1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2825-2841.e10Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no competing interests.