Evidence map›Paper›PMID 32273348›Full record

ReviewJournal for immunotherapy of cancer2020

Lifting the innate immune barriers to antitumor immunity.

Carla V Rothlin, Sourav Ghosh

Abstract readReview
In one paragraph

Review in Journal for immunotherapy of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

  1. Article
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  4. Review
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  8. International journal of molecular sciences · 2025
    Article
  9. Article
  10. Review
  11. Article
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  14. Cold and hot tumors: from molecular mechanisms to targeted therapy.Signal transduction and targeted therapy · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Facts and Hopes in Using Omics to Advance Combined Immunotherapy Strategies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    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

2 authors.

Carla V Rothlin *Immunobiology, Yale School of Medicine, New Haven, CT 06519, United States carla.rothlin@yale.edu sourav.ghosh@yale.edu.
Sourav Ghosh *Pharmacology, Yale School of Medicine, New Haven, CT 06519, United States carla.rothlin@yale.edu sourav.ghosh@yale.edu.

Funding

An innate immune checkpoint in cancer immunotherapy.R01CA212376 · NCI · YALE UNIVERSITY · PI GHOSH, SOURAV, ROTHLIN, CARLA · 2017 to 2021
$3.1M
Howard Hughes Medical Institute 55108561NCI NIH HHS R01 CA212376
6 · The paper itself

Abstract

The immune system evolved for adequate surveillance and killing of pathogens while minimizing host damage, such as due to chronic or exaggerated inflammation and autoimmunity. This is achieved by negative regulators and checkpoints that limit the magnitude and time course of the immune response. Tumor cells often escape immune surveillance and killing. Therefore, disrupting the brakes built into the immune system should effectively boost the anticancer immune response. The success of anti-CTLA4, anti-PD-1 and anti-PD-L1 have firmly established this proof of concept. Since the response rate of anti-CTLA4, anti-PD-1 and anti-PD-L1 is still limited, there is an intense effort for the identification of new targets and development of approaches that can expand the benefits of immunotherapy to a larger patient pool. Additional T cell checkpoints are obvious targets; however, here we focus on the unusual suspects-cells that function to initiate and guide T cell activity. Innate immunity is both an obligate prerequisite for the initiation of adaptive immune responses and a requirement for the recruitment of activated T cells to the site of action. We discuss some of the molecules present in innate immune cells, including natural killer cells, dendritic cells, macrophages, myeloid-derived suppressor cells, endothelial cells and stromal cells, that can activate or enhance innate immune cell functions, and more importantly, the inhibitors or checkpoints present in these cells that restrain their functions. Boosting innate immunity, either by enhancing activator functions or, preferably, by blocking the inhibitors, may represent a new anticancer treatment modality or at least function as adjuvants to T cell checkpoint inhibitors.

Indexed as

HumansImmunity, InnateImmunotherapyNeoplasmsdendritic cellsimmunity, innateinflammationlymphocyte activationmacrophages

Identifiers

PMID32273348
PMCPMC7254113

What OpenQuestion holds

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LicenceCC BY
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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.