Evidence map›Paper›PMID 29114543›Full record

ReviewAnnals of translational medicine2017

Molecular mechanisms of programmed cell death-1 dependent T cell suppression: relevance for immunotherapy.

Miren Zuazo, Maria Gato-Cañas, Noelia Llorente, María Ibañez-Vea, Hugo Arasanz, Grazyna Kochan, David Escors

Open access · hybridAbstract readReview
In one paragraph

Review in Annals of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Article
  8. Gut microbiota affects PD-L1 therapy and its mechanism in melanoma.Cancer immunology, immunotherapy : CII · 2025
    Review
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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

7 authors at 1 institution in 2 countries.

Miren ZuazoBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
Maria Gato-CañasBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
Noelia LlorenteBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
María Ibañez-VeaBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
Hugo ArasanzBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
Grazyna KochanBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
David EscorsBiomedical Research Centre of Navarra-Navarrabiomed, IdISNA, Pamplona 31008, Navarra, Spain.
Navarrabiomed · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Programmed cell death-1 (PD1) has become a significant target for cancer immunotherapy. PD1 and its receptor programmed cell death 1 ligand 1 (PDL1) are key regulatory physiological immune checkpoints that maintain self-tolerance in the organism by regulating the degree of activation of T and B cells amongst other immune cell types. However, cancer cells take advantage of these immunosuppressive regulatory mechanisms to escape T and B cell-mediated immunity. PD1 engagement on T cells by PDL1 on the surface of cancer cells dramatically interferes with T cell activation and the acquisition of effector capacities. Interestingly, PD1-targeted therapies have demonstrated to be highly effective in rescuing T cell anti-tumor effector functions. Amongst these the use of anti-PD1/PDL1 monoclonal antibodies are particularly efficacious in human therapies. Furthermore, clinical findings with PD1/PDL1 blockers over several cancer types demonstrate clinical benefit. Despite the successful results, the molecular mechanisms by which PD1-targeted therapies rescue T cell functions still remain elusive. Therefore, it is a key issue to uncover the molecular pathways by which these therapies exert its function in T cells. A profound knowledge of PDL1/PD1 mechanisms will surely uncover a new array of targets susceptible of therapeutic intervention. Here, we provide an overview of the molecular events underlying PD1-dependent T cell suppression in cancer.

Indexed as

Cancerimmune checkpoint inhibitorsimmunotherapy

Identifiers

PMID29114543
PMCPMC5653513
OpenAlexW2692776313

What OpenQuestion holds

Textmetadata
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.