Evidence map›Paper›PMID 35935956›Full record

ArticleFrontiers in immunology2022

Type II alveolar epithelial cell aryl hydrocarbon receptor protects against allergic airway inflammation through controlling cell autophagy.

Ji Wang, Yilin Zhao, Xin Zhang, Wei Tu, Rongjun Wan, Yingchun Shen, Yan Zhang, Ruchik Trivedi, Peisong Gao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-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

18 citing papers in PubMed, 20 citations in OpenAlex.

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  12. Acute Exposure to Ozone Affects Circulating Estradiol Levels and Gonadotropin Gene Expression in Female Mice.International journal of environmental research and public health · 2025
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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

9 authors at 5 institutions in 2 countries.

Ji WangDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Yilin ZhaoDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Xin ZhangDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Wei TuDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Rongjun WanDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Yingchun ShenDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Yan ZhangDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Ruchik TrivediDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Peisong GaoDivision of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, United States.
Johns Hopkins University · USJohns Hopkins Medicine · USCentral South University · CNWest China Hospital of Sichuan University · CNXijing Hospital · CN

Funding

Environmental Pollutants Potentiate Allergic Inflammation via Functional Axis of Aryl hydrocarbon Receptor, ROS, and CaMKII in AsthmaR01AI141642 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2019 to 2024
$2.9M
Functional role of miR-511-3p in allergic asthma and its underlying mechanismsR01AI153331 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Peisong Gao · 2021 to 2026
$2.7M
NIAID NIH HHS R01 AI141642NIAID NIH HHS R01 AI153331
6 · The paper itself

Abstract

Rationale: Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, has been considered as an important regulator for immune diseases. We have previously shown that AhR protects against allergic airway inflammation. The underlying mechanism, however, remains undetermined. Objectives: We sought to determine whether AhR specifically in type II alveolar epithelial cells (AT2) modulates allergic airway inflammation and its underlying mechanisms. Methods: The role of AhR in AT2 cells in airway inflammation was investigated in a mouse model of asthma with AhR conditional knockout mice in AT2 cells ( Results: Conclusion: These results suggest that AhR in AT2 cells functions as a protective mechanism against allergic airway inflammation through controlling cell autophagy.

Indexed as

AsthmaAllergensAlveolar Epithelial CellsAnimalsAutophagyBasic Helix-Loop-Helix ProteinsChloroquineCytokinesInflammationMiceReceptors, Aryl HydrocarbonAhr protein, mouseAllergensBasic Helix-Loop-Helix ProteinsChloroquineCytokinesReceptors, Aryl Hydrocarbonaryl hydrocarbon receptorasthmaAT2 cellsautophagycockroach allergen

Identifiers

PMID35935956
PMCPMC9355649
OpenAlexW4286685435

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.