PD-1-induced T cell exhaustion is controlled by a Drp1-dependent mechanism.
Drp1
PD-1
T cell
mitochondria
tumor-infiltrating lymphocytes
Journal
Molecular oncology
ISSN: 1878-0261
Titre abrégé: Mol Oncol
Pays: United States
ID NLM: 101308230
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
revised:
30
07
2021
received:
18
02
2021
accepted:
15
09
2021
pubmed:
19
9
2021
medline:
9
4
2022
entrez:
18
9
2021
Statut:
ppublish
Résumé
Programmed cell death-1 (PD-1) signaling downregulates the T-cell response, promoting an exhausted state in tumor-infiltrating T cells, through mostly unveiled molecular mechanisms. Dynamin-related protein-1 (Drp1)-dependent mitochondrial fission plays a crucial role in sustaining T-cell motility, proliferation, survival, and glycolytic engagement. Interestingly, such processes are exactly those inhibited by PD-1 in tumor-infiltrating T cells. Here, we show that PD-1
Identifiants
pubmed: 34535949
doi: 10.1002/1878-0261.13103
pmc: PMC8732338
doi:
Substances chimiques
Pdcd1 protein, mouse
0
Programmed Cell Death 1 Receptor
0
Dnm1l protein, mouse
EC 3.6.5.5
Dynamins
EC 3.6.5.5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
188-205Informations de copyright
© 2021 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
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