Evidence map›Paper›PMID 40395311›Full record

ArticleAutophagy reports2023

External stimulation induces the secretion of autophagosome-like vesicles by B cells.

Yu-Diao Kuan, Chao-Yuan Tsai, Shuhei Sakakibara, Daron M Standley, Hitoshi Kikutani

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Autophagy reports, 2023. 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. Review
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

5 authors.

Yu-Diao KuanDepartment of Genome Informatics, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID https://orcid.org/0000-0002-6591-4706
Chao-Yuan TsaiDepartment of Genome Informatics, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID https://orcid.org/0000-0002-6186-2814
Shuhei SakakibaraDepartment of Genome Informatics, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Daron M StandleyDepartment of Genome Informatics, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, 565-0871, Japan.
Hitoshi KikutaniLaboratory of Immune Regulation, Immunology Frontier Research Center, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID https://orcid.org/0000-0002-2348-3012

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is a cellular degradation and recycling process that supports cellular homeostasis. Since an autophagosome marker, microtubule-associated protein 1A/1B-light chain 3 (LC3)-II, was found in cell-derived extracellular vesicles (EVs), autophagy may cooperate with EV secretion pathways to control unconventional secretion of intracellular molecules. Several studies have demonstrated that pharmacological inhibition of autophagic turnover and pathogen-induced endolysosomal dysfunction enhanced the secretion of autophagosome-like EVs (ALVs). However, whether external stimulation induces ALV secretion is unclear. Here we showed that co-stimulation with IL-4 and anti-CD40 antibody (IL-4:CD40) enhanced the secretion of LC3-II

Indexed as

Autophagosome-like vesiclesB-cell activationCD40 receptorExtracellular vesiclesIL-4RAB27aSecretory autophagy

Identifiers

PMID40395311
PMCPMC12039400

What OpenQuestion holds

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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.