Evidence map›Paper›PMID 25377877›Full record

ArticleDiabetes2015

TLR2- and Dectin 1-associated innate immune response modulates T-cell response to pancreatic β-cell antigen and prevents type 1 diabetes.

Subha Karumuthil-Melethil, M Hanief Sofi, Radhika Gudi, Benjamin M Johnson, Nicolas Perez, Chenthamarakshan Vasu

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

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  9. Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021
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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

6 authors at 2 institutions in 1 country.

Subha Karumuthil-MelethilDepartment of Surgery, University of Illinois at Chicago, Chicago, IL.
M Hanief SofiDepartment of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, SC.
Radhika GudiDepartment of Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC.
Benjamin M JohnsonDepartment of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, SC.
Nicolas PerezDepartment of Surgery, University of Illinois at Chicago, Chicago, IL.
Chenthamarakshan VasuDepartment of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, SC Department of Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC vasu@musc.edu.
Medical University of South Carolina · USUniversity of Illinois Chicago · US

Funding

Dendritic cell directed T cell negative regulation for treating autoimmunityR01AI073858 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI VASU, CHENTHAMARAKSHAN · 2009 to 2013
$1.8M
NIAID NIH HHS R01 AI073858NIAID NIH HHS R01-AI-073858
6 · The paper itself

Abstract

The progression of autoimmune diseases is dictated by deviations in the fine balance between proinflammatory versus regulatory responses, and pathogen recognition receptors (PRRs) play a key role in maintaining this balance. Previously, we have reported that ligation of Toll-like receptor 2 (TLR2) and Dectin 1 on antigen-presenting cells by zymosan results in a regulatory immune response that prevents type 1 diabetes (T1D). Here, we show that TLR2 and Dectin 1 engagement by zymosan promotes regulatory T-cell (Treg) responses against the pancreatic β-cell-specific antigen (Ag). Unlike the TLR4 ligand, bacterial lipopolysaccharide, which induced proinflammatory cytokines and pathogenic T cells, zymosan induced a mixture of pro- and anti-inflammatory factors and Tregs, both in vitro and in vivo. Ag-specific T cells that are activated using zymosan-exposed dendritic cells (DCs) expressed Foxp3 and produced large amounts of IL-10, TGF-β1, and IL-17. NOD mice that received β-cell-Ag-loaded, zymosan-exposed DCs showed delayed hyperglycemia. Injection of NOD mice at the prediabetic age and early hyperglycemic stage with β-cell-Ag, along with zymosan, results in a superior protection of the NOD mice from diabetes as compared with mice that received zymosan alone. This therapeutic effect was associated with increased frequencies of IL-10-, IL-17-, IL-4-, and Foxp3-positive T cells, especially in the pancreatic lymph nodes. These results show that zymosan can be used as an immune regulatory adjuvant for modulating the T-cell response to pancreatic β-cell-Ag and reversing early-stage hyperglycemia in T1D.

Indexed as

AnimalsAntigen-Presenting CellsCytokinesDectin-1Diabetes Mellitus, Type 1Immunity, InnateInsulin-Secreting CellsLectins, C-TypeMiceT-Lymphocytes, RegulatoryToll-Like Receptor 2ZymosanCytokinesDectin-1Lectins, C-TypeTlr2 protein, mouseToll-Like Receptor 2Zymosan

Identifiers

PMID25377877
PMCPMC4375080
OpenAlexW2098000313

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.