Crosslinking of Ly6a metabolically reprograms CD8 T cells for cancer immunotherapy.
Animals
CD8-Positive T-Lymphocytes
/ immunology
Antigens, Ly
/ metabolism
Mice
Immunotherapy
/ methods
Tumor Microenvironment
/ immunology
Mice, Inbred C57BL
Cell Line, Tumor
Humans
Melanoma, Experimental
/ immunology
Female
Programmed Cell Death 1 Receptor
/ metabolism
Skin Neoplasms
/ immunology
Mitochondria
/ metabolism
Melanoma
/ immunology
Interferon Type I
/ metabolism
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
27 Sep 2024
27 Sep 2024
Historique:
received:
13
06
2023
accepted:
25
08
2024
medline:
28
9
2024
pubmed:
28
9
2024
entrez:
27
9
2024
Statut:
epublish
Résumé
T cell inhibitory mechanisms prevent autoimmune reactions, while cancer immunotherapy aims to remove these inhibitory signals. Chronic ultraviolet (UV) exposure attenuates autoimmunity through promotion of poorly understood immune-suppressive mechanisms. Here we show that mice with subcutaneous melanoma are not responsive to anti-PD1 immunotherapy following chronic UV irradiation, given prior to tumor injection, due to the suppression of T cell killing ability in skin-draining lymph nodes. Using mass cytometry and single-cell RNA-sequencing analyzes, we discover that skin-specific, UV-induced suppression of T-cells killing activity is mediated by upregulation of a Ly6a
Identifiants
pubmed: 39333093
doi: 10.1038/s41467-024-52079-x
pii: 10.1038/s41467-024-52079-x
doi:
Substances chimiques
Antigens, Ly
0
Programmed Cell Death 1 Receptor
0
Interferon Type I
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
8354Informations de copyright
© 2024. The Author(s).
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