Evidence map›Paper›PMID 28883439›Full record

ArticleScientific reports2017

T cells display mitochondria hyperpolarization in human type 1 diabetes.

Jing Chen, Anna V Chernatynskaya, Jian-Wei Li, Matthew R Kimbrell, Richard J Cassidy, Daniel J Perry, Andrew B Muir, Mark A Atkinson, Todd M Brusko, Clayton E Mathews

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

  1. Review
  2. Review
  3. Andean Berry (Molecules (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Vitiligo.Nature reviews. Disease primers · 2025
    Review
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  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
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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

10 authors.

Jing ChenDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA. jic24@pathology.ufl.edu.ORCID 0000-0001-8008-8062
Anna V ChernatynskayaDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Jian-Wei LiDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Matthew R KimbrellDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Richard J CassidyDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.ORCID 0000-0003-0019-0679
Daniel J PerryDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Andrew B MuirDepartment of Pediatrics, Emory University, Atlanta, GA, USA.ORCID 0000-0002-4581-9875
Mark A AtkinsonDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Todd M BruskoDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.
Clayton E MathewsDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.

Funding

Project 3P01AI042288 · NIAID · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 1997 to 2026
$32.9M
Genetic Regulation of Human Beta Cell DestructionUC4DK104194 · NIDDK · UNIVERSITY OF FLORIDA · PI MATHEWS, CLAYTON E · 2014 to 2014
$3.1M
mt-Nd2 and Resistance to Autoimmune DiabetesR01DK074656 · NIDDK · UNIVERSITY OF FLORIDA · PI MATHEWS, CLAYTON E · 2006 to 2015
$2.8M
STUDENTS IN HEALTH PROFESSIONAL SCHOOLST35HL007489 · NHLBI · UNIVERSITY OF FLORIDA · PI Scott A Berceli, Robert Maile · 1985 to 2026
$2.4M
NHLBI NIH HHS T35 HL007489NIAID NIH HHS P01 AI042288NIDDK NIH HHS R01 DK074656NIDDK NIH HHS UC4 DK104194
6 · The paper itself

Abstract

T lymphocytes constitute a major effector cell population in autoimmune type 1 diabetes. Despite essential functions of mitochondria in regulating activation, proliferation, and apoptosis of T cells, little is known regarding T cell metabolism in the progression of human type 1 diabetes. In this study, we report, using two independent cohorts, that T cells from patients with type 1 diabetes exhibited mitochondrial inner-membrane hyperpolarization (MHP). Increased MHP was a general phenotype observed in T cell subsets irrespective of prior antigen exposure, and was not correlated with HbA1C levels, subject age, or duration of diabetes. Elevated T cell MHP was not detected in subjects with type 2 diabetes. T cell MHP was associated with increased activation-induced IFNγ production, and activation-induced IFNγ was linked to mitochondria-specific ROS production. T cells from subjects with type 1 diabetes also exhibited lower intracellular ATP levels. In conclusion, intrinsic mitochondrial dysfunction observed in type 1 diabetes alters mitochondrial ATP and IFNγ production; the latter is correlated with ROS generation. These changes impact T cell bioenergetics and function.

Indexed as

Adenosine TriphosphateApoptosisBiomarkersCarbocyaninesDiabetes Mellitus, Type 1GlycolysisHumansImmunophenotypingLymphocyte ActivationMembrane Potential, MitochondrialMicroscopy, ConfocalMitochondriaT-Lymphocyte Subsets3,3'-dihexyl-2,2'-oxacarbocyanineAdenosine TriphosphateBiomarkersCarbocyanines

Identifiers

PMID28883439
PMCPMC5589742

What OpenQuestion holds

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Registered trials

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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.