Evidence map›Paper›PMID 25564999›Full record

ArticleJournal of diabetes2016

Regulation of B lymphocyte responses to Toll-like receptor ligand binding during diabetes prevention in non-obese diabetic (NOD) mice.

Christopher S Wilson, Sydney K Elizer, Andrew F Marshall, Blair T Stocks, Daniel J Moore

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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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 1 institution in 1 country.

Christopher S WilsonDepartment of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA.
Sydney K ElizerDepartment of Pediatrics, Ian Burr Division of Endocrinology and Diabetes, School of Medicine, Vanderbilt University, Nashville, Tennessee, USA.
Andrew F MarshallDepartment of Pediatrics, Ian Burr Division of Endocrinology and Diabetes, School of Medicine, Vanderbilt University, Nashville, Tennessee, USA.
Blair T StocksDepartment of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA.
Daniel J MooreDepartment of Pathology, Microbiology and Immunology, Vanderbilt University, Nashville, Tennessee, USA.
Vanderbilt University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
TRAINING PROGRAM IN CELLULAR, BIOCHEMICAL, &MOLECULAR ST32GM008554 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1995 to 2020
$7.4M
Harnessing B lymphocytes as Antigen-Specific Regulators of Islet ToleranceK08DK090146 · NIDDK · VANDERBILT UNIVERSITY · PI MOORE, DANIEL J. · 2011 to 2013
$434k
NCATS NIH HHS L40 TR000569NIDDK NIH HHS K08 DK090146NIDDK NIH HHS L40 DK084746NIGMS NIH HHS 5T32GM007347-33NIGMS NIH HHS 5T32GM008554-17NIGMS NIH HHS T32 GM007347NIGMS NIH HHS T32 GM008554
6 · The paper itself

Abstract

backgroundInteractions between genetic risk factors and the environment drive type 1 diabetes (T1D). The system of Toll-like receptors (TLR) detects these environmental triggers; however, the target cell that intermediates these interactions to drive T1D remains unknown.

methodsWe investigated the effect of TLR pathway activation (myeloid differentiation primary response 88 [MyD88] vs TIR-domain-containing adapter-inducing interferon-β [TRIF]) on B cell subsets via flow cytometry, including their activation, survival, proliferation, and cytoskeletal mobilization. The effect of polyinosinic-polycytidylic acid (poly(I:C)) on diabetes development was addressed, including the B cell-dependent activation of diabetes-protective DX5+ cells, using genetic models and adoptive transfer.

resultsB lymphocytes from non-obese diabetic (NOD) mice expressed enhanced levels of TLR-responsive proteins. Ex vivo analysis of B lymphocyte subsets demonstrated that TLR3 stimulation via TRIF deletes cells exhibiting a marginal zone phenotype, whereas MyD88-dependent ligands enhance their survival. In vivo, marginal zone B cells were activated by poly(I:C) and were unexpectedly retained in the spleen of NOD mice, in contrast with the mobilization of these cells in non-autoimmune mice, a phenotype we traced to defective actin cytoskeletal dynamics. These activated B cells mediated TLR3-induced diabetes protection.

conclusionsImmunotherapies must account for both B cell location and activation, and these properties may differ in autoimmune and healthy settings.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsAntiviral AgentsB-LymphocytesDiabetes MellitusFemaleFlow CytometryMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDPoly I-CSignal TransductionToll-Like Receptor 3Adaptor Proteins, Vesicular TransportAntiviral AgentsPoly I-CTicam1 protein, mouseTLR3 protein, mouseToll-Like Receptor 31型糖尿病autoimmunityB lymphocyteB淋巴细胞innate immunityToll-like receptorToll样受体type 1 diabetes先天性免疫自身免疫

Identifiers

PMID25564999
PMCPMC4598313
OpenAlexW1910393606

What OpenQuestion holds

Textmetadata
LicenceTDM
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.