Evidence map›Paper›PMID 24973447›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Increased IFN-α-producing plasmacytoid dendritic cells (pDCs) in human Th1-mediated type 1 diabetes: pDCs augment Th1 responses through IFN-α production.

Chang-Qing Xia, Ruihua Peng, Anna V Chernatynskaya, Lihui Yuan, Carolyn Carter, John Valentine, Eric Sobel, Mark A Atkinson, Michael J Clare-Salzler

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 59 citations in OpenAlex.

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  8. Innate immunity in latent autoimmune diabetes in adults.Diabetes/metabolism research and reviews · 2022
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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

9 authors at 1 institution in 1 country.

Chang-Qing XiaDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610;
Ruihua PengDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610;
Anna V ChernatynskayaDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610;
Lihui YuanDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610;
Carolyn CarterDepartment of Pediatrics, University of Florida, Gainesville, FL 32610; and.
John ValentineDepartment of Medicine, University of Florida, Gainesville, FL 32610.
Eric SobelDepartment of Medicine, University of Florida, Gainesville, FL 32610.
Mark A AtkinsonDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610;
Michael J Clare-SalzlerDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610; salzler@pathology.ufl.edu.
University of Florida · US

Funding

Project 3P01AI042288 · NIAID · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 1997 to 2026
$32.9M
Dendritic Cells and the Prevention of Type 1 DiabetesR33DK063422 · NIDDK · UNIVERSITY OF FLORIDA · PI CLARE-SALZLER, MICHAEL JOHN · 2005 to 2007
$1.1M
NIAID NIH HHS P01 AI042288NIDDK NIH HHS R33 DK063422PHS HHS P01 A142288
6 · The paper itself

Abstract

Increasing evidence suggests that type 1 IFN (IFN-αβ) is associated with pathogenesis of Th1-mediated type 1 diabetes (T1D). A major source of IFN-αβ is plasmacytoid dendritic cells (pDCs). In this study, we analyzed peripheral blood pDC numbers and functions in at-risk, new-onset, and established T1D patients and controls. We found that subjects at risk for T1D and new-onset and established T1D subjects possessed significantly increased pDCs but similar number of myeloid DCs when compared with controls. pDC numbers were not affected by age in T1D subjects but declined with increasing age in control subjects. It was demonstrated that IFN-α production by PBMCs stimulated with influenza viruses was significantly higher in T1D subjects than in controls, and IFN-α production was correlated with pDC numbers in PBMCs. Of interest, only T1D-associated Coxsackievirus serotype B4 but not B3 induced majority of T1D PBMCs to produce IFN-α, which was confirmed to be secreted by pDCs. Finally, in vitro studies demonstrated IFN-α produced by pDCs augmented Th1 responses, with significantly greater IFN-γ-producing CD4(+) T cells from T1D subjects. These findings indicate that increased pDCs and their IFN-αβ production may be associated with this Th1-mediated autoimmune disease, especially under certain viral infections linked to T1D pathogenesis.

Indexed as

AdolescentAdultBlood Cell CountCell DifferentiationCells, CulturedChildChild, PreschoolDendritic CellsDiabetes Mellitus, Type 1FemaleHumansInfantInterferon-alphaLeukocytes, MononuclearMaleOrthomyxoviridaeInterferon-alpha

Identifiers

PMID24973447
PMCPMC4500116
OpenAlexW1815216760

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.