IL-33 Induces Sema4A Expression in Dendritic Cells and Exerts Antitumor Immunity.
Animals
Biomarkers
/ metabolism
Carcinoma, Lewis Lung
/ immunology
Cell Differentiation
Dendritic Cells
/ immunology
Disease Models, Animal
Gene Expression Regulation, Neoplastic
Humans
Immunity, Cellular
Interleukin-33
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Neoplasm Transplantation
Semaphorins
/ genetics
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
01 09 2021
01 09 2021
Historique:
received:
25
01
2021
accepted:
01
07
2021
pubmed:
13
8
2021
medline:
7
9
2021
entrez:
12
8
2021
Statut:
ppublish
Résumé
Cancer immunotherapy has shown great promise as a new standard therapeutic strategy against cancer. However, the response rate and survival benefit remain unsatisfactory because most current approaches, such as the use of immune checkpoint inhibitors, depend on spontaneous antitumor immune responses. One possibility for improving the efficacy of immunotherapy is to promote antitumor immunity using adjuvants or specific cytokines actively. IL-33 has been a candidate for such cytokine therapies, but it remains unclear how and in which situations IL-33 exerts antitumor immune effects. In this study, we demonstrate the potent antitumor effects of IL-33 using syngeneic mouse models, which included marked inhibition of tumor growth and upregulation of IFN-γ production by tumor-infiltrating CD8
Identifiants
pubmed: 34380650
pii: jimmunol.2100076
doi: 10.4049/jimmunol.2100076
doi:
Substances chimiques
Biomarkers
0
Interleukin-33
0
Sema4A protein, mouse
0
Semaphorins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1456-1467Informations de copyright
Copyright © 2021 by The American Association of Immunologists, Inc.