Evidence map›Paper›PMID 35300331›Full record

ArticleFrontiers in immunology2022

Human ILC3 Exert TRAIL-Mediated Cytotoxicity Towards Cancer Cells.

Jana-Julia Siegler, Margareta P Correia, Tomáš Hofman, Isabel Prager, Emrullah Birgin, Nuh N Rahbari, Carsten Watzl, Ana Stojanovic, Adelheid Cerwenka

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  15. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    Review
  16. Innate lymphoid cells type 3 in cancer.Frontiers in immunology · 2022
    Review
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

9 authors at 4 institutions in 2 countries.

Jana-Julia SieglerDepartment of Immunobiochemistry, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Margareta P CorreiaDepartment of Immunobiochemistry, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Tomáš HofmanDepartment of Immunobiochemistry, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Isabel PragerDepartment for Immunology, Leibniz Research Centre for Working Environment and Human Factors at TU Dortmund (IfADo), Dortmund, Germany.
Emrullah BirginDepartment of Surgery, University Clinics Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Nuh N RahbariDepartment of Surgery, University Clinics Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Carsten WatzlDepartment for Immunology, Leibniz Research Centre for Working Environment and Human Factors at TU Dortmund (IfADo), Dortmund, Germany.
Ana StojanovicDepartment of Immunobiochemistry, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Adelheid CerwenkaDepartment of Immunobiochemistry, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
University Medical Centre Mannheim · DEHeidelberg University · DETU Dortmund University · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group 3 helper Innate Lymphoid Cells (ILC3s) are cytokine-producing lymphocytes that respond to stress signals released during disturbed tissue homeostasis and infection. Upon activation, ILC3s secrete IL-22 and IL-17, and orchestrate immune responses against extracellular pathogens. Their role in cancer remains poorly explored. To determine their anti-cancer effector potential, we co-cultured cytokine-activated human ILC3s with cancer cells of different origins. ILC3s were able to directly respond to tumor cells, resulting in enhanced IFN-γ production. Upon tumor cell encounter, ILC3s maintained expression of the transcription factor RORγt, indicating that ILC3s preserved their identity. ILC3s were able to directly kill both hepatocellular carcinoma and melanoma tumor cells expressing cell-death receptor TRAILR2, through the activation of Caspase-8 in target cells. Moreover, liver-derived cytokine-activated ILC3s also expressed TRAIL and were able to eliminate hepatoblastoma cells. Together, our data reveal that ILC3s can participate in anti-tumor immune response through direct recognition of tumor cells resulting in IFN-γ release and TRAIL-dependent cytotoxicity. Thus, ILC3s might be ancillary players of anti-tumor immunity in tissues, acting as primary responders against transformed or metastasizing cells, which might be further exploited for therapies against cancer.

Indexed as

LymphocytesNeoplasmsCytokinesGene Expression RegulationHumansImmunity, InnateInterferon-gammaTNF-Related Apoptosis-Inducing LigandCytokinesInterferon-gammaTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humancytotoxicityILCILC3innate immunityNK cellsTRAIL

Identifiers

PMID35300331
PMCPMC8921484
OpenAlexW4214548983

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.