Evidence map›Paper›PMID 30088084›Full record

ArticleMedical microbiology and immunology2019

β-Glucan induces autophagy in dendritic cells and influences T-cell differentiation.

Jun Ding, Yongling Ning, Yu Bai, Ximing Xu, Xiao Sun, Chunjian Qi

Abstract read
PubMed Publisher
In one paragraph

Article in Medical microbiology and immunology, 2019. 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
1.0field-weighted citation impact, top 23% 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, 27 citations in OpenAlex.

  1. Trial
  2. Article
  3. [Isolation, purification and immunomodulatory activity of polysaccharide fromNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
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  12. Immunoenhancing Effects ofJournal of microbiology and biotechnology · 2022
    Article
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  14. Article
  15. Review
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  17. The Macrophage Response toFrontiers in cellular and infection microbiology · 2020
    Review
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.

Jun DingMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital, Nanjing Medical University, Changzhou, 213003, China.
Yongling NingMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital, Nanjing Medical University, Changzhou, 213003, China.
Yu BaiMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital, Nanjing Medical University, Changzhou, 213003, China.
Ximing XuInstitute of Bioinformatics and Medical Engineering, School of Electrical and Information Engineering, Jiangsu University of Technology, Changzhou, China.
Xiao SunMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital, Nanjing Medical University, Changzhou, 213003, China.
Chunjian QiMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital, Nanjing Medical University, Changzhou, 213003, China. qichunjian@njmu.edu.cn.ORCID http://orcid.org/0000-0001-9567-112X
Changzhou No.2 People's Hospital · CNJiangsu University of Technology · CN

Funding

National Natural Science Foundation of China 31500731National Natural Science Foundation of China 81672799
6 · The paper itself

Abstract

β-Glucan has been reported to activate dendritic cells (DCs), and activated DCs, subsequently, promote Th1 and cytotoxic T-lymphocyte priming and differentiation in vitro. However, the mechanism that regulates the immune response of β-glucan-induced DCs has not been thoroughly elucidated to date. Recent studies have drawn attention to a strong relationship between pathogen-associated molecular patterns (PAMP) recognition and autophagy for the activation of DC function. In this study, we observed that β-glucan induced the expression of a number of autophagy-related genes and the formation of autophagosomes in DCs. To further investigate whether β-glucan-induced DC activation and innate cytokine production are associated with autophagy, we utilized 3-MA to block autophagosome formation and accessed the maturation and function of DCs induced by β-glucan. We found that autophagy-deficient DCs showed downregulated expression of MHC-II and CD80, decreased TNF-α secretion, and reduced production of iNOS upon β-glucan stimulation. Further examination demonstrated that blockade of autophagy in β-glucan-induced DCs significantly attenuated IFN-γ production by co-cultured CD4 + T cells and inhibited the proliferation and differentiation of CD4 + T cells. Thus, these data indicate that autophagy in β-glucan-induced DCs is a crucial mechanism for the maturation of DCs, and it drives innate cytokine production, thereby facilitating adaptive immune responses.

Indexed as

Cell DifferentiationAnimalsAutophagybeta-GlucansCD4-Positive T-LymphocytesCells, CulturedCytokinesDendritic CellsMice, Inbred C57BLbeta-GlucansCytokinesAutophagyDendritic cellsT-cell differentiationβ-Glucan

Identifiers

PMID30088084
OpenAlexW2887782370

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.