Evidence map›Paper›PMID 24465383›Full record

ArticlePloS one2014

Involvement of suppressive B-lymphocytes in the mechanism of tolerogenic dendritic cell reversal of type 1 diabetes in NOD mice.

Valentina Di Caro, Brett Phillips, Carl Engman, Jo Harnaha, Massimo Trucco, Nick Giannoukakis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Epitope-based precision immunotherapy of Type 1 diabetes.Human vaccines & immunotherapeutics · 2023
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  14. Article
  15. Regulatory B cells and transplantation: almost prime time?Current opinion in organ transplantation · 2018
    Review
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  17. Article
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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 1 country.

Valentina Di CaroDivision of Immunogenetics, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America ; RiMed Foundation, Palermo, Italy.
Brett PhillipsPenn State University Hershey Medical Center, Hershey, Pennsylvania, United States of America.
Carl EngmanDivision of Immunogenetics, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
Jo HarnahaDivision of Immunogenetics, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
Massimo TruccoDivision of Immunogenetics, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
Nick GiannoukakisDivision of Immunogenetics, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America ; Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
University of Pittsburgh · USPenn State Milton S. Hershey Medical Center · US

Funding

Gene-engineered dendritic cell therapy for diabeticsR33DK063499 · NIDDK · CHILDREN'S HOSP PITTSBURGH/UPMC HLTH SYS · PI TRUCCO, MASSIMO M. · 2005 to 2006
$1.0M
Gene-engineered dendritic cell therapy for diabeticsR21DK063499 · NIDDK · CHILDREN'S HOSP PITTSBURGH/UPMC HLTH SYS · PI TRUCCO, MASSIMO M. · 2002 to 2003
$571k
NIDDK NIH HHS DK063499NIDDK NIH HHS R21 DK063499NIDDK NIH HHS R33 DK063499
6 · The paper itself

Abstract

The objective of the study was to identify immune cell populations, in addition to Foxp3+ T-regulatory cells, that participate in the mechanisms of action of tolerogenic dendritic cells shown to prevent and reverse type 1 diabetes in the Non-Obese Diabetic (NOD) mouse strain. Co-culture experiments using tolerogenic dendritic cells and B-cells from NOD as well as transgenic interleukin-10 promoter-reporter mice along with transfer of tolerogenic dendritic cells and CD19+ B-cells into NOD and transgenic mice, showed that these dendritic cells increased the frequency and numbers of interleukin-10-expressing B-cells in vitro and in vivo. The expansion of these cells was a consequence of both the proliferation of pre-existing interleukin-10-expressing B-lymphocytes and the conversion of CD19+ B-lymphcytes into interleukin-10-expressing cells. The tolerogenic dendritic cells did not affect the suppressive activity of these B-cells. Furthermore, we discovered that the suppressive murine B-lymphocytes expressed receptors for retinoic acid which is produced by the tolerogenic dendritic cells. These data assist in identifying the nature of the B-cell population increased in response to the tolerogenic dendritic cells in a clinical trial and also validate very recent findings demonstrating a mechanistic link between human tolerogenic dendritic cells and immunosuppressive regulatory B-cells.

Indexed as

Immune ToleranceAnimalsAntigens, CD19B-LymphocytesCell ProliferationDendritic CellsDiabetes Mellitus, Type 1FemaleFlow CytometryHumansHyperglycemiaImmunomodulationInterleukin-10Lymphocyte ActivationLymphocyte Culture Test, MixedMiceAntigens, CD19Interleukin-10Oligonucleotides, AntisenseReceptors, Retinoic Acid

Identifiers

PMID24465383
PMCPMC3894962
OpenAlexW1974893432

What OpenQuestion holds

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LicenceCC BY
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.