Evidence map›Paper›PMID 25287445›Full record

ReviewImmunology and cell biology2015

Autophagy in T-cell development, activation and differentiation.

Alisha W Bronietzki, Marc Schuster, Ingo Schmitz

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Immunology and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 115 citations in OpenAlex.

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12 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.

Alisha W Bronietzki1] Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany [2] Institute for Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
Marc Schuster1] Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany [2] Institute for Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
Ingo Schmitz1] Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany [2] Institute for Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
Helmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a vital catabolic process for degrading bulky cytosolic contents, which cannot be resorbed via the proteasome. First described as a survival mechanism during nutrient starvation conditions, recent reports have demonstrated that autophagy supports metabolic functions of T cells at various stages of maturation and effector function. Autophagy is crucial for T-cell development at the precursor stage as self-renewability and quiescence of hematopoietic stem cells depend on autophagy of the mitochondria and the endoplasmic reticulum. Later, during development in the thymus, autophagy regulates peptide presentation in stromal cells and professional antigen-presenting cells, which mediate thymocyte selection. Furthermore, the metabolic changes when mature T cells enter the periphery and when they are activated are both dependent on autophagy. Lastly, autophagy prevents early aging and, thus, ensures maintenance of memory T cells.

Indexed as

AgingAnimalsAntigen PresentationApoptosis Regulatory ProteinsAutophagyCell DifferentiationDendritic CellsGene Expression Regulation, DevelopmentalHematopoietic Stem CellsHumansImmunologic MemoryLymphocyte ActivationMitochondriaPhagosomesThymus GlandT-LymphocytesApoptosis Regulatory ProteinsUbiquitin-Conjugating Enzymes

Identifiers

PMID25287445
OpenAlexW2083440174

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.