Evidence map›Paper›PMID 40977681›Full record

ArticleFrontiers in immunology2025

Loss of ATG5 impairs CD4+ T cell activation and promotes anti-tumor responses.

Carlos Plaza-Sirvent, Clara Bessen, Alisha W Bronietzki, Katjana Klages, Marc Schuster, Jochen Huehn, Ingo Schmitz

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Carlos Plaza-SirventDept. of Molecular Immunology, Ruhr University Bochum, Bochum, Germany.
Clara BessenDept. of Molecular Immunology, Ruhr University Bochum, Bochum, Germany.
Alisha W BronietzkiSystems-oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Katjana KlagesDepartment of Experimental Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Marc SchusterSystems-oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Jochen HuehnDepartment of Experimental Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Ingo SchmitzDept. of Molecular Immunology, Ruhr University Bochum, Bochum, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy (hereafter called autophagy) is an ancient catabolic process that delivers bulky cargo to lysosomal degradation. The autophagic pathway is regulated by autophagy-related (ATG) proteins that govern the formation of double-membraned vesicles called autophagosomes. Autophagy has been shown to be important for T cell survival and proliferation. However, all studies performed so far used genetic models, in which deletion of an essential

Indexed as

Autophagy-Related Protein 5CD4-Positive T-LymphocytesLymphocyte ActivationAnimalsAutophagyMiceMice, Inbred C57BLMice, KnockoutT-Lymphocytes, RegulatoryAtg5 protein, mouseAutophagy-Related Protein 5ATG5autophagyCD4 T cellregulatory T cellT cell activation

Identifiers

PMID40977681
PMCPMC12443542

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.