Evidence map›Paper›PMID 35461286›Full record

ArticleCell & bioscience2022

Aryl hydrocarbon receptor activation ameliorates experimental colitis by modulating the tolerogenic dendritic and regulatory T cell formation.

Xiufang Cui, Ziping Ye, Di Wang, Yan Yang, ChunHua Jiao, Jingjing Ma, Nana Tang, Hongjie Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

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  12. Frontiers in immunology · 2025
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  17. Aryl Hydrocarbon Receptor Signalling in the Control of Gut Inflammation.International journal of molecular sciences · 2024
    Review
  18. Article
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  20. Observational
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

8 authors at 2 institutions in 1 country.

Xiufang Cui *Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China.
Ziping Ye *Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China.
Di WangDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China.
Yan YangDepartment of Gastroenterology, Sir Run Run Hospital, Nanjing Medical University, Nanjing, 211100, Jiangsu, People's Republic of China.
ChunHua JiaoDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China.
Jingjing MaDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China.
Nana TangDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China.
Hongjie ZhangDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300# Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China. hjzhang06@163.com.ORCID http://orcid.org/0000-0003-4497-0503
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

National Natural Science Foundation of China 81770553National Natural Science Foundation of China 82070568Postgraduate Research & Practice Innovation Program of Jiangsu Province JX10213640
6 · The paper itself

Abstract

backgroundIntestinal immune dysfunction is involved in the onset of Crohn's disease (CD). Dendritic cells (DCs), antigen-presenting cells, play a key role in the maintenance of intestinal immune homeostasis. The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor widely expressed in various immune cells, including DCs. Although AhR plays an important role in immune tolerance, its role in the DCs is unclear. The purpose of this study was to investigate whether the activation of AhR can induce tolerogenic DCs (tolDCs) and the differentiation of regulatory T (Treg) cells, as well as ameliorate experimental colitis.

resultsAhR activation in the DCs resulted in a lower expression of surface markers such as CD80, CD83, CD86, and pro-inflammatory cytokine production, and higher anti-inflammatory production (IL-1β, IL-23, and IL-12) compared to the control DCs. The surface dendrites in DCs were significantly reduced following AhR activation by 6-formylindolo [3,2-b]carbazole (FICZ). Such DCs with FICZ-mediated activation of AhR, namely tolDCs, promoted Treg cell differentiation. Adoptive transfer of tolDCs to a TNBS-induced colitis mouse model significantly alleviated the severity of inflammation by improving the colon length and decreasing the disease activity index (DAI) and histopathological score. Moreover, the transferred tolDCs decreased the frequency of Th17 cells and increased the frequency of Treg cells in the spleen and mesenteric lymph nodes (MLNs) in murine colitis models.

conclusionsActivation of AhR in the DCs could induce tolDCs, and the transplantation of tolDCs may help in relieving intestinal inflammation and maintaining the Th17/Treg differentiation balance. Thus, our data suggest that AhR may be a potential therapeutic target for CD.

Indexed as

Aryl hydrocarbon receptorCrohn’s diseaseDendritic cellsIntestinal immune toleranceTreg cells

Identifiers

PMID35461286
PMCPMC9034494
OpenAlexW4224657301

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.