Evidence map›Paper›PMID 30406374›Full record

ReviewCancer immunology, immunotherapy : CII2019

Apoptosis of tumor-infiltrating T lymphocytes: a new immune checkpoint mechanism.

Jingjing Zhu, Pierre-Florent Petit, Benoit J Van den Eynde

Open access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
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  11. Biomedicines · 2025
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  20. CD8Journal of translational medicine · 2024
    Review

17 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Jingjing ZhuLudwig Institute for Cancer Research, 1200, Brussels, Belgium.
Pierre-Florent PetitLudwig Institute for Cancer Research, 1200, Brussels, Belgium.
Benoit J Van den EyndeLudwig Institute for Cancer Research, 1200, Brussels, Belgium. benoit.vandeneynde@bru.licr.org.ORCID http://orcid.org/0000-0002-4995-3270
Ludwig Cancer Research · BE

Funding

Fonds De La Recherche Scientifique - FNRS 1.A.818.18
6 · The paper itself

Abstract

Immunotherapy based on checkpoint inhibitors is providing substantial clinical benefit, but only to a minority of cancer patients. The current priority is to understand why the majority of patients fail to respond. Besides T-cell dysfunction, T-cell apoptosis was reported in several recent studies as a relevant mechanism of tumoral immune resistance. Several death receptors (Fas, DR3, DR4, DR5, TNFR1) can trigger apoptosis when activated by their respective ligands. In this review, we discuss the immunomodulatory role of the main death receptors and how these are shaping the tumor microenvironment, with a focus on Fas and its ligand. Fas-mediated apoptosis of T cells has long been known as a mechanism allowing the contraction of T-cell responses to prevent immunopathology, a phenomenon known as activation-induced cell death, which is triggered by induction of Fas ligand (FasL) expression on T cells themselves and qualifies as an immune checkpoint mechanism. Recent evidence indicates that other cells in the tumor microenvironment can express FasL and trigger apoptosis of tumor-infiltrating lymphocytes (TIL), including endothelial cells and myeloid-derived suppressor cells. The resulting disappearance of TIL prevents anti-tumor immunity and may in fact contribute to the absence of TIL that is typical of "cold" tumors that fail to respond to immunotherapy. Interfering with the Fas-FasL pathway in the tumor microenvironment has the potential to increase the efficacy of cancer immunotherapy.

Indexed as

AnimalsAntibodies, MonoclonalApoptosisCostimulatory and Inhibitory T-Cell ReceptorsFas Ligand Proteinfas ReceptorHumansImmunotherapyLymphocytes, Tumor-InfiltratingNeoplasmsSignal TransductionT-LymphocytesAntibodies, MonoclonalCostimulatory and Inhibitory T-Cell ReceptorsFas Ligand ProteinFAS protein, humanfas ReceptorCancer immunotherapyDeath receptorsFas ligandMDSCPIVAC 17TIL apoptosis

Identifiers

PMID30406374
PMCPMC11028327
OpenAlexW2900048176

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.