Evidence map›Paper›PMID 24037540›Full record

ArticleEuropean journal of immunology2013

Mitochondrial and cytosolic roles of PINK1 shape induced regulatory T-cell development and function.

Gavin I Ellis, Lianteng Zhi, Ravi Akundi, Hansruedi Büeler, Francesc Marti

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Effect of mitochondrial oxidative stress on regulatory T cell manufacturing for clinical application in transplantation: Results from a pilot study.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Article
  5. Article
  6. Article
  7. PINK1 is a target of T cell responses in Parkinson's disease.bioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. T Lymphocytes in Parkinson's Disease.Journal of Parkinson's disease · 2022
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Immunometabolism of pro-repair cells.The Journal of clinical investigation · 2019
    Review
  18. Article
  19. Article
  20. 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 at 1 institution in 1 country.

Gavin I EllisDepartment of Microbiology, Immunology & Molecular Genetics, University of Kentucky College of Medicine, Lexington, KY, USA.
Lianteng Zhi
Ravi Akundi
Hansruedi Büeler
Francesc Marti
University of Kentucky · US

Funding

UNDERSTANDING THE MOLECULAR BASIS OF EPIGENETIC TRANSCRIPTIONAL SILENCINGP20RR020171 · NCRR · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2004 to 2011
$16.5M
Cell Sorter Upgrade for Flow Cytometry Service FacilityS10RR026827 · NCRR · UNIVERSITY OF KENTUCKY · PI COHEN, DONALD A · 2011 to 2011
$600k
NCRR NIH HHS P20 RR020171NCRR NIH HHS S10 RR026827NCRR NIH HHS S10 RR026827-01A1
6 · The paper itself

Abstract

Mutations in PTEN-induced kinase 1 (PINK1), a serine/threonine kinase linked to familial early-onset Parkinsonism, compromise mitochondrial integrity and metabolism and impair AKT signaling. As the activation of a naïve T cell requires an AKT-dependent reorganization of a cell's metabolic machinery, we sought to determine if PINK1-deficient T cells lack the ability to undergo activation and differentiation. We show that CD4(+) T cells from PINK1 knockout mice fail to properly phosphorylate AKT upon activation, resulting in reduced expression of the IL-2 receptor subunit CD25. Following, deficient IL-2 signaling mutes the activation-induced increase in respiratory capacity and mitochondrial membrane potential. Under polarization conditions favoring the development of induced regulatory T cells, PINK1(-/-) T cells exhibit a reduced ability to suppress bystander T-cell proliferation despite normal FoxP3 expression kinetics. Our results describe a critical role for PINK1 in integrating extracellular signals with metabolic state during T-cell fate determination, and may have implications for the understanding of altered T-cell populations and immunity during the progression of active Parkinson's disease or other immunopathologies.

Indexed as

Lymphocyte ActivationAnimalsCell DifferentiationCytosolForkhead Transcription FactorsHumansInterleukin-2Interleukin-2 Receptor alpha SubunitMiceMice, KnockoutMitochondriaParkinson DiseasePhosphorylationProtein KinasesProto-Oncogene Proteins c-aktPTEN-Induced Putative KinaseForkhead Transcription FactorsFoxp3 protein, mouseInterleukin-2Interleukin-2 Receptor alpha SubunitProtein KinasesProto-Oncogene Proteins c-aktPTEN-Induced Putative KinaseAKT signalingParkinson's diseasePeripheral T‐cell differentiationRegulatory T (Treg) cellsT‐cell signaling

Identifiers

PMID24037540
PMCPMC4539263
OpenAlexW1623634791

What OpenQuestion holds

Textmetadata
LicenceTDM
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.