Evidence map›Paper›PMID 24315098›Full record

ArticleCell2013

A special population of regulatory T cells potentiates muscle repair.

Dalia Burzyn, Wilson Kuswanto, Dmitriy Kolodin, Jennifer L Shadrach, Massimiliano Cerletti, Young Jang, Esen Sefik, Tze Guan Tan, Amy J Wagers, Christophe Benoist and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 782 papers.

0numbers the graph read from it
0cells of the map it votes in
782citing papers in PubMed
26.0field-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

782 citing papers in PubMed, 1,159 citations in OpenAlex.

  1. Article
  2. Regulatory T cells: From Foxp3 to tolerance-inducing therapies.The Journal of investigative dermatology · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
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  8. Article
  9. A who's who of cell types in skeletal muscle.Communications biology · 2026
    Review
  10. Review
  11. Review
  12. Article
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  14. Article
  15. Article
  16. Review
  17. T-betThe FEBS journal · 2026
    Article
  18. Review
  19. Article
  20. Article

722 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Dalia BurzynMicrobiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Wilson Kuswanto
Dmitriy Kolodin
Jennifer L Shadrach
Massimiliano Cerletti
Young Jang
Esen Sefik
Tze Guan Tan
Amy J Wagers
Christophe Benoist
Diane Mathis
Harvard University · USHoward Hughes Medical Institute · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
Microenvironmental control of progenitors in organ dysfunction and repairU01HL100402 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI KIM, CARLA F., SCADDEN, DAVID T · 2009 to 2015
$8.5M
Adipose-tissue Tregs: important players in immunological control of metabolismR01DK092541 · NIDDK · HARVARD MEDICAL SCHOOL · PI DIANE J MATHIS · 2011 to 2026
$6.4M
Naive T cell homeostasis: Treg selection and survivalR37AI051530 · NIAID · HARVARD MEDICAL SCHOOL · PI BENOIST, CHRISTOPHE O. · 2009 to 2018
$4.1M
Reversing age-related dysfunction of skeletal muscle stem cellsR01AG033053 · NIA · JOSLIN DIABETES CENTER · PI WAGERS, AMY JO · 2009 to 2014
$2.0M
Howard Hughes Medical InstituteNHLBI NIH HHS U01 HL100402NHLBI NIH HHS U01HL100402NIAID NIH HHS R37 AI051530NIAID NIH HHS R37AI051530NIA NIH HHS R01 AG033053NIA NIH HHS R01AG033053NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30DK036836NIDDK NIH HHS R01 DK092541NIDDK NIH HHS R01DK092541
6 · The paper itself

Abstract

Long recognized to be potent suppressors of immune responses, Foxp3(+)CD4(+) regulatory T (Treg) cells are being rediscovered as regulators of nonimmunological processes. We describe a phenotypically and functionally distinct population of Treg cells that rapidly accumulated in the acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switched from a proinflammatory to a proregenerative state. A Treg population of similar phenotype accumulated in muscles of genetically dystrophic mice. Punctual depletion of Treg cells during the repair process prolonged the proinflammatory infiltrate and impaired muscle repair, while treatments that increased or decreased Treg activities diminished or enhanced (respectively) muscle damage in a dystrophy model. Muscle Treg cells expressed the growth factor Amphiregulin, which acted directly on muscle satellite cells in vitro and improved muscle repair in vivo. Thus, Treg cells and their products may provide new therapeutic opportunities for wound repair and muscular dystrophies.

Indexed as

RegenerationAmphiregulinAnimalsEGF Family of ProteinsGlycoproteinsIntercellular Signaling Peptides and ProteinsLymphoid TissueMiceMice, Inbred C57BLMuscle, SkeletalMuscular DystrophiesReceptors, Antigen, T-CellT-Lymphocytes, RegulatoryTranscriptomeAmphiregulinAreg protein, mouseEGF Family of ProteinsGlycoproteinsIntercellular Signaling Peptides and ProteinsReceptors, Antigen, T-Cell

Identifiers

PMID24315098
PMCPMC3894749
OpenAlexW2151328705

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.