Evidence map›Paper›PMID 24218453›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Antigen-specific induced T regulatory cells impair dendritic cell function via an IL-10/MARCH1-dependent mechanism.

Gouri Chattopadhyay, Ethan M Shevach

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. CD137-expressing regulatory T cells in cancer and autoimmune diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. IL-10Frontiers in immunology · 2021
    Article
  15. Regulatory T Cells in Chronic Heart Failure.Frontiers in immunology · 2021
    Review
  16. Overcoming Immune Evasion in Melanoma.International journal of molecular sciences · 2020
    Review
  17. Review
  18. Article
  19. Review
  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

2 authors at 2 institutions in 1 country.

Gouri ChattopadhyayLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Ethan M Shevach
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Studies of the Function of Naturally Occurring and Adaptive T Regulatory CellsZIAAI000959 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHEVACH, ETHAN · 2009 to 2025
$17.6M
Control of Autoimmunity by Regulatory T CellsZIAAI000224 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHEVACH, ETHAN · 2009 to 2025
$13.4M
RECEPTORS, CORECEPTORS, AND COUNTER RECEPTORS IN T CELL ACTIVATIONZ01AI000224 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHEVACH, ETHAN M. · 1985 to 2008
$3.5M
Intramural NIH HHS Z01 AI000224
6 · The paper itself

Abstract

Foxp3(+) T regulatory cells (Tregs) are critically important for the maintenance of immunological tolerance, immune homeostasis, and prevention of autoimmunity. Dendritic cells (DCs) are one of the major targets of Treg-mediated suppression. Some studies have suggested that Treg-mediated suppression of DC function is mediated by the interaction of CTLA-4 on Tregs with CD80/CD86 on the DCs resulting in downregulation of CD80/CD86 expression and a decrease in costimulation. We have re-examined the effects of Tregs on mouse DC function in a model in which Ag-specific, induced Tregs (iTregs) are cocultured with DCs in the absence of T effector cells. iTreg-treated DCs are markedly defective in their capacity to activate naive T cells. iTregs from CTLA-4-deficient mice failed to induce downregulation of CD80/CD86, but DCs treated with CTLA-4-deficient iTregs still exhibited impaired capacity to activate naive T cells. The iTreg-induced defect in DC function could be completely reversed by anti-IL-10, and IL-10-deficient iTregs failed to downregulate DC function. iTreg-treated DCs expressed high levels of MARCH1, an E3 ubiquitin ligase, recently found to degrade CD86 and MHC class II on the DCs and expressed lower levels of CD83, a molecule involved in neutralizing the function of MARCH1. Both the enhanced expression of MARCH1 and the decreased expression of CD83 were mediated by IL-10 produced by the iTregs. Taken together, these studies demonstrate that a major suppressive mechanism of DC function by iTregs is secondary to the effects of IL-10 on MARCH1 and CD83 expression.

Indexed as

T-Cell Antigen Receptor SpecificityAnimalsAntigen PresentationAntigens, CDB7-1 AntigenB7-2 AntigenCD4-Positive T-LymphocytesCD83 AntigenCells, CulturedCell SeparationCoculture TechniquesCTLA-4 AntigenDendritic CellsDNA-Binding ProteinsEpitopes, T-LymphocyteFlow CytometryAntigens, CDB7-1 AntigenB7-2 AntigenCD83 AntigenCd86 protein, mouseCTLA-4 AntigenCtla4 protein, mouseDNA-Binding ProteinsEpitopes, T-LymphocyteHistocompatibility Antigens Class IIIL10 protein, mouseImmunoglobulinsInterleukin-10MARCH1 protein, mouseMembrane GlycoproteinsRag2 protein, mouseRNA, MessengerUbiquitin-Protein Ligases

Identifiers

PMID24218453
PMCPMC3858537
OpenAlexW2151693216

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.