Human primed ILCPs support endothelial activation through NF-κB signaling.

Details

Ressource 1Request a copy Sous embargo indéterminé.
State: Public
Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_1C654EDB478E
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Human primed ILCPs support endothelial activation through NF-κB signaling.
Journal
eLife
Author(s)
Vanoni G., Ercolano G., Candiani S., Rutigliani M., Lanata M., Derré L., Marcenaro E., Schneider P., Romero P., Jandus C., Trabanelli S.
ISSN
2050-084X (Electronic)
ISSN-L
2050-084X
Publication state
Published
Issued date
08/02/2021
Peer-reviewed
Oui
Volume
10
Pages
e58838
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Innate lymphoid cells (ILCs) represent the most recently identified subset of effector lymphocytes, with key roles in the orchestration of early immune responses. Despite their established involvement in the pathogenesis of many inflammatory disorders, the role of ILCs in cancer remains poorly defined. Here we assessed whether human ILCs can actively interact with the endothelium to promote tumor growth control, favoring immune cell adhesion. We show that, among all ILC subsets, ILCPs elicited the strongest upregulation of adhesion molecules in endothelial cells (ECs) in vitro, mainly in a contact-dependent manner through the tumor necrosis factor receptor- and RANK-dependent engagement of the NF-κB pathway. Moreover, the ILCP-mediated activation of the ECs resulted to be functional by fostering the adhesion of other innate and adaptive immune cells. Interestingly, pre-exposure of ILCPs to human tumor cell lines strongly impaired this capacity. Hence, the ILCP-EC interaction might represent an attractive target to regulate the immune cell trafficking to tumor sites and, therefore, the establishment of an anti-tumor immune response.
Keywords
NF-κB, cancer biology, endothelium, human, immunology, inflammation, innate lymphoid cells
Pubmed
Web of science
Open Access
Yes
Create date
22/02/2021 14:21
Last modification date
08/07/2021 5:36
Usage data