Evidence map›Paper›PMID 33554861›Full record

ArticleeLife2021

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

Giulia Vanoni, Giuseppe Ercolano, Simona Candiani, Mariangela Rutigliani, Mariangela Lanata, Laurent Derré, Emanuela Marcenaro, Pascal Schneider, Pedro Romero, Camilla Jandus and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Giulia VanoniDepartment of Oncology, Ludwig Institute for Cancer Research - University of Lausanne, Lausanne, Switzerland.ORCID 0000-0003-3199-2412
Giuseppe ErcolanoDepartment of Oncology, Ludwig Institute for Cancer Research - University of Lausanne, Lausanne, Switzerland.
Simona CandianiDepartment of Earth Science, Environment and Life, University of Genova, Genova, Italy.
Mariangela RutiglianiDepartment of Laboratory and Service, Histological and Anatomical Pathology, E.O. Galliera Hospital, Genova, Italy.
Mariangela LanataDepartment of Laboratory and Service, Histological and Anatomical Pathology, E.O. Galliera Hospital, Genova, Italy.
Laurent DerréDepartment of Urology, University Hospital of Lausanne (CHUV), Lausanne, Switzerland.
Emanuela MarcenaroDepartment of Experimental Medicine and Centre of Excellence for Biomedical Research, University of Genova, Genova, Italy.
Pascal SchneiderDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Pedro RomeroDepartment of Oncology, University of Lausanne, Lausanne, Switzerland.
Camilla JandusDepartment of Oncology, Ludwig Institute for Cancer Research - University of Lausanne, Lausanne, Switzerland.
Sara TrabanelliDepartment of Oncology, Ludwig Institute for Cancer Research - University of Lausanne, Lausanne, Switzerland.ORCID 0000-0001-8648-1324
Ludwig Cancer Research · CHEnte Ospedaliero Ospedali Galliera · ITUniversity of Genoa · ITUniversity of Lausanne · CHUniversity Hospital of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Cell Adhesion MoleculesEndothelial CellsEndotheliumHumansImmunity, InnateLymphocytesNF-kappa BReceptors, Tumor Necrosis FactorCell Adhesion MoleculesNF-kappa BReceptors, Tumor Necrosis Factorcancer biologyendotheliumhumanimmunologyinflammationinnate lymphoid cellsNF-κB

Identifiers

PMID33554861
PMCPMC7891932
OpenAlexW3127699154

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.