Evidence map›Paper›PMID 17197428›Full record

ArticleBlood2007

New differentiation pathway for double-negative regulatory T cells that regulates the magnitude of immune responses.

Dong Zhang, Wei Yang, Nicolas Degauque, Yan Tian, Allison Mikita, Xin Xiao Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

72 citing papers in PubMed, 125 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Characterization of circulating CD4International journal of hematology · 2017
    Trial
  4. Article
  5. Double negative T cells (CD4Frontiers in immunology · 2026
    Article
  6. Article
  7. Increased CD95Frontiers in immunology · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Characterization and effective expansion of CD4Molecular therapy. Methods & clinical development · 2025
    Article
  12. Purinergic signaling by TCRαβScience bulletin · 2025
    Article
  13. CD3Frontiers in immunology · 2025
    Review
  14. Article
  15. Double-negative T cells in pediatric rheumatic diseases.Clinical and experimental pediatrics · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Canine peripheral non-conventional TCRαβFrontiers in immunology · 2024
    Article

12 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

6 authors at 2 institutions in 2 countries.

Dong ZhangTransplantation Research Center, Beth Israel Deaconess Medical Center, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Wei Yang
Nicolas Degauque
Yan Tian
Allison Mikita
Xin Xiao Zheng
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have demonstrated that in peripheral lymphoid tissues of normal mice and healthy humans, 1% to 5% of alphabeta T-cell receptor-positive (TCR(+)) T cells are CD4(-)CD8(-) (double-negative [DN]) T cells, capable of down-regulating immune responses. However, the origin and developmental pathway of DN T cells is still not clear. In this study, by monitoring CD4 expression during T-cell proliferation and differentiation, we identified a new differentiation pathway for the conversion of CD4(+) T cells to DN regulatory T cells. We showed that the converted DN T cells retained a stable phenotype after restimulation and that furthermore, the disappearance of cell-surface CD4 molecules on converted DN T cells was a result of CD4 gene silencing. The converted DN T cells were resistant to activation-induced cell death (AICD) and expressed a unique set of cell-surface markers and gene profiles. These cells were highly potent in suppressing alloimmune responses both in vitro and in vivo in an antigen-specific manner. Perforin was highly expressed by the converted DN regulatory T cells and played a role in DN T-cell-mediated suppression. Our findings thus identify a new differentiation pathway for DN regulatory T cells and uncover a new intrinsic homeostatic mechanism that regulates the magnitude of immune responses. This pathway provides a novel, cell-based, therapeutic approach for preventing allograft rejection.

Indexed as

Cell ProliferationAnimalsCD4 AntigensCD8 AntigensCell DeathCell DifferentiationGene SilencingHomeostasisIsoantigensMembrane GlycoproteinsMiceMice, KnockoutPerforinPore Forming Cytotoxic ProteinsReceptors, Antigen, T-Cell, alpha-betaT-Lymphocytes, RegulatoryCD4 AntigensCD8 AntigensIsoantigensMembrane GlycoproteinsPerforinPore Forming Cytotoxic ProteinsReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID17197428
PMCPMC1874581
OpenAlexW2009116479

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.