Evidence map›Paper›PMID 23426179›Full record

ArticleThe Journal of clinical investigation2013

Depletion of FOXP3+ regulatory T cells promotes hypercholesterolemia and atherosclerosis.

Roland Klingenberg, Norbert Gerdes, Robert M Badeau, Anton Gisterå, Daniela Strodthoff, Daniel F J Ketelhuth, Anna M Lundberg, Mats Rudling, Stefan K Nilsson, Gunilla Olivecrona and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
212citing papers in PubMed, 2 pooled it
17.3field-weighted citation impact, top 1% 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

212 citing papers in PubMed, 2 syntheses or guidelines pooled it, 363 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Trial
  4. Trial
  5. Trial
  6. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  7. Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Loss of effector TNature cardiovascular research · 2025
    Article
  17. Article
  18. Review
  19. Review
  20. Review

152 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

16 authors at 7 institutions in 4 countries.

Roland KlingenbergCenter for Molecular Medicine, Department of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
Norbert Gerdes
Robert M Badeau
Anton Gisterå
Daniela Strodthoff
Daniel F J Ketelhuth
Anna M Lundberg
Mats Rudling
Stefan K Nilsson
Gunilla Olivecrona
Stefan Zoller
Christine Lohmann
Thomas F Lüscher
Matti Jauhiainen
Tim Sparwasser
Göran K Hansson
Karolinska University Hospital · SEUmeå University · SEUniversity of Zurich · CHCenter for Experimental and Clinical Infection Research · DEETH Zurich · CHInstitute for Molecular Medicine Finland · FIKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease promoted by hyperlipidemia. Several studies support FOXP3-positive regulatory T cells (Tregs) as inhibitors of atherosclerosis; however, the mechanism underlying this protection remains elusive. To define the role of FOXP3-expressing Tregs in atherosclerosis, we used the DEREG mouse, which expresses the diphtheria toxin (DT) receptor under control of the Treg-specific Foxp3 promoter, allowing for specific ablation of FOXP3+ Tregs. Lethally irradiated, atherosclerosis-prone, low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice received DEREG bone marrow and were injected with DT to eliminate FOXP3(+) Tregs. Depletion of Tregs caused a 2.1-fold increase in atherosclerosis without a concomitant increase in vascular inflammation. These mice also exhibited a 1.7-fold increase in plasma cholesterol and an atherogenic lipoprotein profile with increased levels of VLDL. Clearance of VLDL and chylomicron remnants was hampered, leading to accumulation of cholesterol-rich particles in the circulation. Functional and protein analyses complemented by gene expression array identified reduced protein expression of sortilin-1 in liver and increased plasma enzyme activity of lipoprotein lipase, hepatic lipase, and phospholipid transfer protein as mediators of the altered lipid phenotype. These results demonstrate that FOXP3(+) Tregs inhibit atherosclerosis by modulating lipoprotein metabolism.

Indexed as

AnimalsAortaAtherosclerosisCells, CulturedForkhead Transcription FactorsHypercholesterolemiaLipaseLipid MetabolismLipidsLipoproteins, VLDLLiverLymphocyte DepletionMaleMiceMice, Inbred C57BLMice, TransgenicForkhead Transcription FactorsFoxp3 protein, mouseLipaseLipidsLipoproteins, VLDLphospholipid transfer protein, mousePhospholipid Transfer ProteinsReceptors, LDL

Identifiers

PMID23426179
PMCPMC3582120
OpenAlexW2027516092

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.