Evidence map›Paper›PMID 30518692›Full record

ArticleJCI insight2018

CD19+IgM+ cells demonstrate enhanced therapeutic efficacy in type 1 diabetes mellitus.

Andrew D Vonberg, Maria Acevedo-Calado, Aaron R Cox, Susan L Pietropaolo, Roberto Gianani, Steven K Lundy, Massimo Pietropaolo

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
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.

Andrew D VonbergDiabetes Research Center, Division of Diabetes, Endocrinology and Metabolism Department of Medicine, and.
Maria Acevedo-CaladoDiabetes Research Center, Division of Diabetes, Endocrinology and Metabolism Department of Medicine, and.
Aaron R CoxDiabetes Research Center, Division of Diabetes, Endocrinology and Metabolism Department of Medicine, and.
Susan L PietropaoloDiabetes Research Center, Division of Diabetes, Endocrinology and Metabolism Department of Medicine, and.
Roberto GiananiDiabetes Research Center, Division of Diabetes, Endocrinology and Metabolism Department of Medicine, and.
Steven K LundyDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Massimo PietropaoloDiabetes Research Center, Division of Diabetes, Endocrinology and Metabolism Department of Medicine, and.
Diabetes Research CenterBaylor College of Medicine · USUniversity of Michigan · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
NIAID NIH HHS T32 AI007413NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

We describe a protective effect on autoimmune diabetes and reduced destructive insulitis in NOD.scid recipients following splenocyte injections from diabetic NOD donors and sorted CD19+ cells compared with NOD.scid recipients receiving splenocytes alone. This protective effect was age specific (only CD19+ cells from young NOD donors exerted this effect; P < 0.001). We found that the CD19+IgM+ cell is the primary subpopulation of B cells that delayed transfer of diabetes mediated by diabetogenic T cells from NOD mice (P = 0.002). Removal of IgM+ cells from the CD19+ pool did not result in protection. Notably, protection conferred by CD19+IgM+ cotransfers were not dependent on the presence of Tregs, as their depletion did not affect their ability to delay onset of diabetes. Blockade of IL-10 with neutralizing antibodies at the time of CD19+ cell cotransfers also abrogated the therapeutic effect, suggesting that IL-10 secretion was an important component of protection. These results were strengthened by ex vivo incubation of CD19+ cells with IL-5, resulting in enhanced proliferation and IL-10 production and equivalently delayed diabetes progression (P = 0.0005). The potential to expand CD19+IgM+ cells, especially in response to IL-5 stimulation or by pharmacologic agents, may be a new therapeutic option for type 1 diabetes.

Indexed as

AnimalsAntibodies, NeutralizingAntigens, CD19B-LymphocytesCell ProliferationDiabetes Mellitus, Type 1FemaleHistocompatibility Antigens Class IImmunoglobulin MInterleukin-10Interleukin-5MiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, SCIDAntibodies, NeutralizingAntigens, CD19CD19 antigen, mouseHistocompatibility Antigens Class IImmunoglobulin MInterleukin-10Interleukin-5AutoimmunityB cellsImmunology

Identifiers

PMID30518692
PMCPMC6328032
OpenAlexW2903137315

What OpenQuestion holds

Textmetadata
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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.