Immunosuppressive Mediators Impair Proinflammatory Innate Lymphoid Cell Function in Human Malignant Melanoma.

Details

Serval ID
serval:BIB_61DAEC10A322
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Immunosuppressive Mediators Impair Proinflammatory Innate Lymphoid Cell Function in Human Malignant Melanoma.
Journal
Cancer immunology research
Author(s)
Ercolano G., Garcia-Garijo A., Salomé B., Gomez-Cadena A., Vanoni G., Mastelic-Gavillet B., Ianaro A., Speiser D.E., Romero P., Trabanelli S., Jandus C.
ISSN
2326-6074 (Electronic)
ISSN-L
2326-6066
Publication state
Published
Issued date
04/2020
Peer-reviewed
Oui
Volume
8
Number
4
Pages
556-564
Language
english
Notes
Publication types: Journal Article
Publication Status: ppublish
Abstract
Innate lymphoid cells (ILC) are a family of immune cells that are emerging as potent orchestrators of immune responses. In cancer, ILCs display both pro- and antitumorigenic functions depending on the nature of the tumor and the involved ILC subset. Little is known about the ILC-tumor cross-talk in human melanoma. Here, we showed that ILC1s were enriched but functionally impaired in cytokine secretion in both peripheral blood mononuclear cells and tumor-infiltrated lymph nodes of melanoma patients. These findings were confirmed in vivo in murine cutaneous melanoma. Multiple immunosuppressive mechanisms are described in the melanoma microenvironment. Among others, adenosine and kynurenines were shown to suppress antitumor immune responses. By exposing ILCs to adenosine and kynurenines, we observed a similar shift toward the ILC1 subset distribution and impairment in proinflammatory cytokine production to that of patient samples studied ex vivo. Thus, we hypothesized that the immunosuppressive microenvironment of malignant melanoma might shape ILC subpopulations. Hence, we provide a rationale for the use of drugs targeting adenosine and kynurenine pathways in melanoma patients.
Pubmed
Web of science
Open Access
Yes
Create date
06/02/2020 18:14
Last modification date
23/11/2020 7:24
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