Evidence map›Paper›PMID 31728048›Full record

ArticleCellular & molecular immunology2020

Dendritic cells license regulatory B cells to produce IL-10 and mediate suppression of antigen-specific CD8 T cells.

Joanne Boldison, Larissa Camargo Da Rosa, Joanne Davies, Li Wen, F Susan Wong

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Article
  7. Expansion of B10 cellsInternational journal of molecular medicine · 2025
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  9. Article
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  15. Epitope-based precision immunotherapy of Type 1 diabetes.Human vaccines & immunotherapeutics · 2023
    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

5 authors at 2 institutions in 2 countries.

Joanne BoldisonDivision of Infection and Immunity, Cardiff University School of Medicine, Cardiff, CF14 4XN, UK.
Larissa Camargo Da RosaDivision of Infection and Immunity, Cardiff University School of Medicine, Cardiff, CF14 4XN, UK.
Joanne DaviesDivision of Infection and Immunity, Cardiff University School of Medicine, Cardiff, CF14 4XN, UK.
Li WenSection of Endocrinology, School of Medicine, Yale University, Yale, CT, 06520, USA.
F Susan WongDivision of Infection and Immunity, Cardiff University School of Medicine, Cardiff, CF14 4XN, UK. WongFS@Cardiff.ac.uk.
Cardiff University · GBYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold, GERALD I SHULMAN · 1993 to 2026
$44.0M
Investigating the early development of the immune system and islet autoimmunity later in lifeR01HD097808 · NICHD · YALE UNIVERSITY · PI WEN, LI · 2019 to 2021
$1.3M
ROLE OF NUCLEAR SCAFFOLD PROTEASE IN CARCINOGENESISR01CA021141 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CLAWSON, GARY A · 1985 to 1998
–
Medical Research Council MR/K021141/1NCATS NIH HHS UL1 TR001863NICHD NIH HHS R01 HD097808NIDDK NIH HHS P30 DK045735
6 · The paper itself

Abstract

Regulatory B cells (Bregs) suppress and reduce autoimmune pathology. However, given the variety of Breg subsets, the role of Bregs in the pathogenesis of type 1 diabetes is still unclear. Here, we dissect this fundamental mechanism. We show that natural protection from type 1 diabetes in nonobese diabetic (NOD) mice is associated with increased numbers of IL-10-producing B cells, while development of type 1 diabetes in NOD mice occurs in animals with compromised IL-10 production by B cells. However, B cells from diabetic mice regain IL-10 function if activated by the innate immune receptor TLR4 and can suppress insulin-specific CD8 T cells in a dendritic cell (DC)-dependent, IL-10-mediated fashion. Suppression of CD8 T cells is reliant on B-cell contact with DCs. This cell contact results in deactivation of DCs, inducing a tolerogenic state, which in turn can regulate pathogenic CD8 T cells. Our findings emphasize the importance of DC-Breg interactions during the development of type 1 diabetes.

Indexed as

Immunosuppression TherapyAnimalsAntigens, CDB-Lymphocytes, RegulatoryCD8-Positive T-LymphocytesCell DifferentiationCytokinesDendritic CellsDiabetes Mellitus, Type 1EpitopesImmune ToleranceInsulinInterleukin-10LipopolysaccharidesMice, Inbred NODModels, ImmunologicalAntigens, CDCytokinesEpitopesInsulinInterleukin-10LipopolysaccharidesDendritic cellsIL-10Regulatory B cellstype 1 diabetes

Identifiers

PMID31728048
PMCPMC7395736
OpenAlexW2986250088

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.