Evidence map›Paper›PMID 25143443›Full record

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

Fungal β-glucan, a Dectin-1 ligand, promotes protection from type 1 diabetes by inducing regulatory innate immune response.

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

Open access · bronzeAbstract 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 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.4field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 85 citations in OpenAlex.

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  4. Nutrients · 2024
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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 2 institutions in 1 country.

Subha Karumuthil-MelethilDepartment of Surgery, University of Illinois at Chicago, Chicago, IL 60612;
Radhika GudiDepartment of Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC 29425; and.
Benjamin M JohnsonDepartment of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, SC 29425.
Nicolas PerezDepartment of Surgery, University of Illinois at Chicago, Chicago, IL 60612;
Chenthamarakshan VasuDepartment of Surgery, University of Illinois at Chicago, Chicago, IL 60612; Department of Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC 29425; and Department of Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, SC 29425 vasu@musc.edu.
University of Illinois Chicago · USMedical University of South Carolina · 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 R01AI073858
6 · The paper itself

Abstract

β-Glucans are naturally occurring polysaccharides in cereal grains, mushrooms, algae, or microbes, including bacteria, fungi, and yeast. Immune cells recognize these β-glucans through a cell surface pathogen recognition receptor called Dectin-1. Studies using β-glucans and other Dectin-1 binding components have demonstrated the potential of these agents in activating the immune cells for cancer treatment and controlling infections. In this study, we show that the β-glucan from Saccharomyces cerevisiae induces the expression of immune regulatory cytokines (IL-10, TGF-β1, and IL-2) and a tolerogenic enzyme (IDO) in bone marrow-derived dendritic cells as well as spleen cells. These properties can be exploited to modulate autoimmunity in the NOD mouse model of type 1 diabetes (T1D). Treatment of prediabetic NOD mice with low-dose β-glucan resulted in a profound delay in hyperglycemia, and this protection was associated with increase in the frequencies of Foxp3(+), LAP(+), and GARP(+) T cells. Upon Ag presentation, β-glucan-exposed dendritic cells induced a significant increase in Foxp3(+) and LAP(+) T cells in in vitro cultures. Furthermore, systemic coadministration of β-glucan plus pancreatic β cell Ag resulted in an enhanced protection of NOD mice from T1D as compared with treatment with β-glucan alone. These observations demonstrate that the innate immune response induced by low-dose β-glucan is regulatory in nature and can be exploited to modulate T cell response to β cell Ag for inducing an effective protection from T1D.

Indexed as

Animalsbeta-GlucansCytokinesDectin-1Dendritic CellsDiabetes Mellitus, Type 1Dose-Response Relationship, ImmunologicFungal PolysaccharidesImmunity, InnateInsulin-Secreting CellsLectins, C-TypeMiceMice, Inbred NODMice, SCIDMice, TransgenicSaccharomyces cerevisiaebeta-GlucansCytokinesDectin-1Fungal PolysaccharidesLectins, C-Type

Identifiers

PMID25143443
PMCPMC4170060
OpenAlexW1933209079

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.