Evidence map›Paper›PMID 24082013›Full record

ArticleJournal of leukocyte biology2014

CD8+ dendritic cell-mediated tolerance of autoreactive CD4+ T cells is deficient in NOD mice and can be corrected by blocking CD40L.

Jeffrey D Price, Nicole M Beauchamp, Gwendoline Rahir, Yongge Zhao, Cosima C Rieger, Annie W Lau-Kilby, Kristin V Tarbell

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Innate immunity in latent autoimmune diabetes in adults.Diabetes/metabolism research and reviews · 2022
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
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  15. Article
  16. The Importance of Dendritic Cells in Maintaining Immune Tolerance.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Review
  17. Review
  18. Review
  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

7 authors at 2 institutions in 1 country.

Jeffrey D Price1.Diabetes, Endocrinology, and Obesity Branch, NIDDK, NIH, Bldg. 10, CRC, West Labs, 5-5940, Bethesda, MD 20892, USA. tarbellk@niddk.nih.gov.
Nicole M Beauchamp
Gwendoline Rahir
Yongge Zhao
Cosima C Rieger
Annie W Lau-Kilby
Kristin V Tarbell
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Targeting antigen to dendritic cells in autoimmune diabetesZIADK075065 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI TARBELL, KRISTIN · 2012 to 2017
$3.2M
Intramural NIH HHS
6 · The paper itself

Abstract

DCs are important mediators of peripheral tolerance for the prevention of autoimmunity. Chimeric αDEC-205 antibodies with attached antigens allow in vivo antigen-specific stimulation of T cells by CD8(+) DCs, resulting in tolerance in nonautoimmune mice. However, it is not clear whether DC-mediated tolerance induction occurs in the context of ongoing autoimmunity. We assessed the role of CD8(+) DCs in stimulation of autoreactive CD4(+) T cells in the NOD mouse model of type 1 diabetes. Targeting of antigen to CD8(+) DCs via αDEC-205 led to proliferation and expansion of β-cell specific BDC2.5 T cells. These T cells also produced IL-2 and IFN-γ and did not up-regulate FoxP3, consistent with an activated rather than tolerant phenotype. Similarly, endogenous BDC peptide-reactive T cells, identified with I-A(g7) tetramers, did not become tolerant after antigen delivery via αDEC-205: no deletion or Treg induction was observed. We observed that CD8(+) DCs from NOD mice expressed higher surface levels of CD40 than CD8(+) DCs from C57BL/6 mice. Blockade of CD40-CD40L interactions reduced the number of BDC2.5 T cells remaining in mice, 10 days after antigen targeting to CD8 DCs, and blocked IFN-γ production by BDC2.5 T cells. These data indicate that the ability of autoreactive CD4(+) T cells to undergo tolerance mediated by CD8(+) DCs is defective in NOD mice and that blocking CD40-CD40L interactions can restore tolerance induction.

Indexed as

AnimalsAntibodiesAntigensCD40 AntigensCD40 LigandCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationDendritic CellsDiabetes Mellitus, ExperimentalForkhead Transcription FactorsImmune ToleranceInterferon-gammaLigandsLymphocyte ActivationMiceAntibodiesAntigensCD40 AntigensCD40 LigandForkhead Transcription FactorsFoxp3 protein, mouseInterferon-gammaLigandsPeptidesToll-Like ReceptorsCD40DEC-205peripheral tolerancetype 1 diabetes

Identifiers

PMID24082013
PMCPMC3896656
OpenAlexW2119058174

What OpenQuestion holds

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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.