Evidence map›Paper›PMID 20625402›Full record

ArticlePloS one2010

Double negative (CD3+ 4- 8-) TCR alphabeta splenic cells from young NOD mice provide long-lasting protection against type 1 diabetes.

Beverly Duncan, Cristina Nazarov-Stoica, Jacqueline Surls, Margaret Kehl, Constantin Bona, Sofia Casares, Teodor-D Brumeanu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  4. Neuroprotective role of DNTαβ Cell transplantation on modulating immune microenvironment in spinal cord injured mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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  7. Characterization and effective expansion of CD4Molecular therapy. Methods & clinical development · 2025
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  8. Association of TCRαβFrontiers in immunology · 2025
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  9. CD3Frontiers in immunology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. CD3Frontiers in immunology · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

7 authors at 3 institutions in 1 country.

Beverly DuncanNational Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Cristina Nazarov-Stoica
Jacqueline Surls
Margaret Kehl
Constantin Bona
Sofia Casares
Teodor-D Brumeanu
Uniformed Services University of the Health Sciences · USIcahn School of Medicine at Mount Sinai · USNational Cancer Institute · US

Funding

Prevention Type 1 diabetes by soluble, MHC II-peptideR01DK061927 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BRUMEANU, TEODOR-DORU BRUMEANU · 2001 to 2005
$800k
NEGATIVE REGULATION OF AUTOREACTIVE T-CELLSR21DK061326 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BRUMEANU, TEODOR-DORU BRUMEANU · 2001 to 2003
$627k
Immunokinetics of Autoreactive CD4 T cells in Blood as Biomarker for T1DR21DK077521 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CASARES, SOFIA · 2006 to 2007
$419k
NIDDK NIH HHS DK077521NIDDK NIH HHS DK61326NIDDK NIH HHS DK61927NIDDK NIH HHS R01 DK061927NIDDK NIH HHS R21 DK061326NIDDK NIH HHS R21 DK077521
6 · The paper itself

Abstract

backgroundDouble negative CD3(+)4(-)8(-) TCR alphabeta splenic cells (DNCD3) can suppress the immune responses to allo and xenografts, infectious agents, tumors, and some autoimmune disorders. However, little is known about their role in autoimmune diabetes, a disease characterized by the reduction of insulin production subsequent to destruction of pancreatic beta-cells by a polyclonal population of self-reactive T-cells. Herein, we analyzed the function and phenotype of DNCD3 splenic cells in young NOD mice predisposed to several autoimmune disorders among which, the human-like autoimmune diabetes. METHODOLOGY/PRINCIPAL

findingsDNCD3 splenic cells from young NOD mice (1) provided long-lasting protection against diabetes transfer in NOD/Scid immunodeficient mice, (2) proliferated and differentiated in the spleen and pancreas of NOD/Scid mice and pre-diabetic NOD mice into IL-10-secreting T(R)-1 like cells in a Th2-like environment, and (3) their anti-diabetogenic phenotype is CD3(+)(CD4(-)CD8(-))CD28(+)CD69(+)CD25(low) Foxp3(-) iCTLA-4(-)TCR alphabeta(+) with a predominant Vbeta13 gene usage. CONCLUSIONS/SIGNIFICANCE: These findings delineate a new T regulatory component in autoimmune diabetes apart from that of NKT and CD4(+)CD25(high) Foxp3(+)T-regulatory cells. DNCD3 splenic cells could be potentially manipulated towards the development of autologous cell therapies in autoimmune diabetes.

Indexed as

AnimalsCD3 ComplexCD4 AntigensCD8 AntigensCell CycleCell ProliferationCells, CulturedDiabetes Mellitus, Type 1Flow CytometryImmunohistochemistryMiceMice, Inbred NODMice, SCIDReceptors, Antigen, T-Cell, alpha-betaReverse Transcriptase Polymerase Chain ReactionSpleenCD3 ComplexCD4 AntigensCD8 AntigensReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID20625402
PMCPMC2896421
OpenAlexW2039050866

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Registered trials

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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.