Evidence map›Paper›PMID 19768696›Full record

ArticleEuropean journal of immunology2009

Novel CD8+ Treg suppress EAE by TGF-beta- and IFN-gamma-dependent mechanisms.

Mei-Ling Chen, Bo-Shiun Yan, Deneen Kozoriz, Howard L Weiner

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Characterization of novel CD8Cellular and molecular life sciences : CMLS · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. CD8Frontiers in immunology · 2020
    Review
  10. Future prospects for CD8Immunological reviews · 2019
    Review
  11. Extracellular vesicle fibrinogen induces encephalitogenic CD8+ T cells in a mouse model of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Description of CD8Journal of immunology research · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Mei-Ling ChenCenter for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. mlingchen@rics.bwh.harvard.edu
Bo-Shiun Yan
Deneen Kozoriz
Howard L Weiner
Brigham and Women's Hospital · USHarvard University · US

Funding

The function of T Bet in EAEP01NS038037 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2000 to 2010
$12.8M
MECHANISMS OF THE INDUCTION OF ORAL TOLERANCER01AI043458 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 1998 to 2015
$5.0M
NIAID NIH HHS R01 AI043458NINDS NIH HHS P01 NS038037
6 · The paper itself

Abstract

Although CD8+ Treg-mediated suppression has been described, CD8+ Treg remain poorly characterized. Here we identify a novel subset of CD8+ Treg that express latency-associated peptide (LAP) on their cell surface (CD8+LAP+ cells) and exhibit regulatory activity in vitro and in vivo. Only a small fraction of CD8+LAP+ cells express Foxp3 or CD25, although the expression levels of Foxp3 for these cells are higher than their LAP- counterparts. In addition to TGF-beta, CD8+LAP+ cells produce IFN-gamma, and these cells suppress EAE that is dependent on both TGF-beta and IFN-gamma. In an adoptive co-transfer model, CD8+LAP+ cells suppress myelin oligodendrocyte glycoprotein (MOG)-specific immune responses by inducing or expanding Foxp3+ cells and by inhibiting proliferation and IFN-gamma production in vivo. Furthermore, in vivo neutralization of IFN-gamma and studies with IFN-gamma-deficient mice demonstrate an important role for IFN-gamma production in the function of CD8+LAP+ cells. Our findings identify the underlying mechanisms that account for the immunoregulatory activity of CD8+ T cells and suggest that induction or amplification of CD8+LAP+ cells may be a therapeutic strategy to help control autoimmune processes.

Indexed as

Adoptive TransferAnalysis of VarianceAnimalsCD8 AntigensCD8-Positive T-LymphocytesCytokinesEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFemaleForkhead Transcription FactorsGlycoproteinsInterferon-gammaInterferon gamma ReceptorInterleukin-2 Receptor alpha SubunitMiceMice, Inbred C57BLCD8 AntigensCytokinesForkhead Transcription FactorsFoxp3 protein, mouseGlycoproteinsInterferon-gammaInterferon gamma ReceptorInterleukin-2 Receptor alpha SubunitMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Myelin ProteinsPeptide FragmentsReceptors, InterferonTransforming Growth Factor beta

Identifiers

PMID19768696
PMCPMC2814307
OpenAlexW1969281065

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.