Evidence map›Paper›PMID 26124756›Full record

ReviewFrontiers in immunology2015

The Role of Dendritic Cell Subsets and Innate Immunity in the Pathogenesis of Type 1 Diabetes and Other Autoimmune Diseases.

Jeffrey D Price, Kristin V Tarbell

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
–field-weighted citation impact
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

51 citing papers in PubMed.

  1. Trial
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  7. Sex as a modifier of genetic risk for type 1 diabetes.Diabetes, obesity & metabolism · 2025
    Review
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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

2 authors.

Jeffrey D PriceDiabetes, Endocrinology, and Obesity Branch, Immune Tolerance Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, MD , USA.
Kristin V TarbellDiabetes, Endocrinology, and Obesity Branch, Immune Tolerance Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, MD , USA.

Funding

dendrtitic cell subsets in autoimmune diabetesZIADK069014 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI TARBELL, KRISTIN · 2009 to 2017
$5.6M
Targeting antigen to dendritic cells in autoimmune diabetesZIADK075065 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI TARBELL, KRISTIN · 2012 to 2017
$3.2M
6 · The paper itself

Abstract

Dendritic cells (DCs) are key antigen-presenting cells that have an important role in autoimmune pathogenesis. DCs control both steady-state T cell tolerance and activation of pathogenic responses. The balance between these two outcomes depends on several factors, including genetic susceptibility, environmental signals that stimulate varied innate responses, and which DC subset is presenting antigen. Although the specific DC phenotype can diverge depending on the tissue location and context, there are four main subsets identified in both mouse and human: conventional cDC1 and cDC2, plasmacytoid DCs, and monocyte-derived DCs. In this review, we will discuss the role of these subsets in autoimmune pathogenesis and regulation, as well as the genetic and environmental signals that influence their function. Specific topics to be addressed include impact of susceptibility loci on DC subsets, alterations in DC subset development, the role of infection- and host-derived innate inflammatory signals, and the role of the intestinal microbiota on DC phenotype. The effects of these various signals on disease progression and the relative effects of DC subset composition and maturation level of DCs will be examined. These areas will be explored using examples from several autoimmune diseases but will focus mainly on type 1 diabetes.

Indexed as

antigen presentationautoimmunitydendritic cellsinnate immunityT cell tolerancetype 1 diabetes

Identifiers

PMID26124756
PMCPMC4466467

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Registered trials

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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.