Evidence map›Paper›PMID 32849515›Full record

ReviewFrontiers in immunology2020

The AHR Signaling Attenuates Autoimmune Responses During the Development of Type 1 Diabetes.

Tiantian Yue, Fei Sun, Chunliang Yang, Faxi Wang, Jiahui Luo, Ping Yang, Fei Xiong, Shu Zhang, Qilin Yu, Cong-Yi Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  6. Vaccines · 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

10 authors at 2 institutions in 1 country.

Tiantian YueCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fei SunCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Chunliang YangCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Faxi WangCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jiahui LuoCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ping YangCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fei XiongCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Shu ZhangCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Qilin YuCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Cong-Yi WangCenter for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Tongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcriptional factor widely expressed in immune cells. Its ligands range from xenobiotics and natural substances to metabolites, which renders it capable of sensing and responding to a variety of environmental cues. Although AHR signaling has long been recognized to be implicated in the pathogenesis of autoimmune disorders, such as rheumatoid arthritis (RA), colitis, and systemic lupus erythematosus (SLE), its effect on the pathogenesis of type 1 diabetes (T1D) remains less understood. In this review, we intend to summarize its potential implication in T1D pathogenesis and to sort out the related regulatory mechanisms in different types of immune cells. Emerging evidence supports that β cell destruction caused by autoimmune responses can be rectified by AHR signaling. Upon activation by its ligands, AHR not only modulates the development and functionality of immune cells, but also suppresses the expression of inflammatory cytokines, through which AHR attenuates autoimmune responses during the course of T1D development. Since AHR-initiated biological effects vary between different types of ligands, additional studies would be necessary to characterize or

Indexed as

AnimalsAutoimmunityDiabetes Mellitus, Type 1HumansInsulin-Secreting CellsMolecular Targeted TherapyReceptors, Aryl HydrocarbonSignal TransductionReceptors, Aryl HydrocarbonAHR Ligandsaryl hydrocarbon receptorimmune responseT1Dtherapeutic target

Identifiers

PMID32849515
PMCPMC7426364
OpenAlexW3047884319

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.