Evidence map›Paper›PMID 31484658›Full record

ArticleCancer immunology research2019

The Atypical Receptor CCRL2 Is Essential for Lung Cancer Immune Surveillance.

Annalisa Del Prete, Francesca Sozio, Tiziana Schioppa, Andrea Ponzetta, William Vermi, Stefano Calza, Mattia Bugatti, Valentina Salvi, Giovanni Bernardini, Federica Benvenuti and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer immunology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Multiscale Computational Dissection of CCRL2-Mediated Chemerin Presentation.Journal of chemical information and modeling · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Combinatorial chemistry & high throughput screening · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. An integrated model for predicting KRAS dependency.PLoS computational biology · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

14 authors at 5 institutions in 3 countries.

Annalisa Del PreteDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Francesca SozioDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Tiziana SchioppaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.ORCID https://orcid.org/0000-0002-6303-6065
Andrea PonzettaIRCCS Humanitas Clinical and Research Center, Rozzano, Italy.ORCID https://orcid.org/0000-0003-3224-802X
William VermiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Stefano CalzaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Mattia BugattiDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Valentina SalviDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Giovanni BernardiniDepartment of Molecular Medicine, Sapienza University of Rome, Laboratory Affiliated to Institute Pasteur-Italia, Rome, Italy.
Federica BenvenutiInternational Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Annunciata VecchiIRCCS Humanitas Clinical and Research Center, Rozzano, Italy.
Barbara BottazziIRCCS Humanitas Clinical and Research Center, Rozzano, Italy.
Alberto MantovaniIRCCS Humanitas Clinical and Research Center, Rozzano, Italy.ORCID https://orcid.org/0000-0001-5578-236X
Silvano SozzaniDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. silvano.sozzani@unibs.it.ORCID https://orcid.org/0000-0002-3144-8743
Humanitas University · ITUniversity of Brescia · ITInternational Centre for Genetic Engineering and Biotechnology · ITIstituto Neurologico Mediterraneo · ITKarolinska Institutet · SE

Funding

European Research Council 669415
6 · The paper itself

Abstract

CCRL2 is a nonsignaling seven-transmembrane domain receptor. CCRL2 binds chemerin, a protein that promotes chemotaxis of leukocytes, including macrophages and natural killer (NK) cells. In addition, CCRL2 controls the inflammatory response in different pathologic settings, such as hypersensitivity, inflammatory arthritis, and experimental autoimmune encephalitis. Here, we investigated the role of CCRL2 in the regulation of lung cancer-related inflammation. The genetic deletion of

Indexed as

Immunologic SurveillanceAnimalsCell Line, TumorChemotaxis, LeukocyteDisease Models, AnimalDisease ProgressionEndothelial CellsHumansKiller Cells, NaturalLung NeoplasmsMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, CCRSurvival AnalysisCcrl2 protein, mouseReceptors, CCR

Identifiers

PMID31484658
PMCPMC7176487
OpenAlexW2972289577

What OpenQuestion holds

Textmetadata
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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.