The myeloid cell type I IFN system promotes antitumor immunity over pro-tumoral inflammation in cancer T-cell therapy.
adaptive resistance
cancer immunotherapy
hypoxia
melanoma plasticity
myeloid cells
type I interferon
Journal
Clinical & translational immunology
ISSN: 2050-0068
Titre abrégé: Clin Transl Immunology
Pays: Australia
ID NLM: 101638268
Informations de publication
Date de publication:
2021
2021
Historique:
received:
21
11
2019
revised:
24
08
2020
revised:
10
12
2020
revised:
02
03
2021
accepted:
25
03
2021
entrez:
10
5
2021
pubmed:
11
5
2021
medline:
11
5
2021
Statut:
epublish
Résumé
Type I interferons are evolutionally conserved cytokines, with broad antimicrobial and immunoregulatory functions. Despite well-characterised role in spontaneous cancer immunosurveillance, the function of type I IFNs in cancer immunotherapy remains incompletely understood. We utilised genetic mouse models to explore the role of the type I IFN system in CD8 The therapeutic efficacy of adoptively transferred T cells was found to depend on a functional type I IFN system in myeloid immune cells. Compromised type I IFN signalling in myeloid immune cells did not prevent expansion, tumor infiltration or effector function of melanoma-specific Pmel-1 CD8 Our results substantiate a complex and plastic phenotypic interconnection between melanoma and myeloid cells in the context of T-cell immunotherapy. Type I IFN signalling in myeloid cells was identified as a key regulator of the balance between antitumor immunity and disease-promoting inflammation, thus supporting the development of novel combinatorial immunotherapies targeting this immune cell compartment.
Identifiants
pubmed: 33968406
doi: 10.1002/cti2.1276
pii: CTI21276
pmc: PMC8082713
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e1276Informations de copyright
© 2021 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology, Inc.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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