Evidence map›Paper›PMID 36369368›Full record

ArticleCellular & molecular immunology2022

Aryl hydrocarbon receptor activation drives polymorphonuclear myeloid-derived suppressor cell response and efficiently attenuates experimental Sjögren's syndrome.

Yanxia Wei, Na Peng, Chong Deng, Futao Zhao, Jie Tian, Yuan Tang, Sulan Yu, Yacun Chen, Yu Xue, Fan Xiao and 6 more

Open access · greenAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
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  4. Myeloid-Derived Suppressor Cells in Inflammatory Arthritis.International journal of molecular sciences · 2026
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 9 institutions in 3 countries.

Yanxia Wei *Department of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Na Peng *Department of Rheumatology, the Second People's Hospital, China Three Gorges University, Yichang, China.
Chong DengDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Futao ZhaoDepartment of Rheumatology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jie TianDepartment of Laboratory Medicine, Affiliated Hospital and Institute of Medical Immunology, Jiangsu University, Zhenjiang, China.ORCID 0000-0003-4182-3495
Yuan TangDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Sulan YuSchool of Chinese Medicine and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Yacun ChenSchool of Chinese Medicine and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Yu XueDepartment of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China.
Fan XiaoDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Yingbo ZhouDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Xiaomei LiDepartment of Rheumatology and Immunology, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, Anhui, China.
Hejian ZouDepartment of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China.
Ke RuiDepartment of Laboratory Medicine, Affiliated Hospital and Institute of Medical Immunology, Jiangsu University, Zhenjiang, China. ruike@ujs.edu.cn.
Xiang LinSchool of Chinese Medicine and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China. linxiang@hku.hk.
Liwei LuDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China. liweilu@hku.hk.ORCID 0000-0002-8634-0967
Chinese University of Hong Kong, Shenzhen · CNCity University of Hong Kong, Shenzhen Research Institute · CNFudan University · CNHong Kong Science and Technology Parks Corporation · HKJiangsu University · CNChina Three Gorges University · CNShanghai Jiao Tong University · CNUniversity of Science and Technology of China · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) comprise heterogeneous myeloid cell populations with immunosuppressive capacity that contribute to immune regulation and tolerance induction. We previously reported impaired MDSC function in patients with primary Sjögren's syndrome (pSS) and mice with experimental SS (ESS). However, the molecular mechanisms underlying MDSC dysfunction remain largely unclear. In this study, we first found that aryl hydrocarbon receptor (AhR) was highly expressed by human and murine polymorphonuclear MDSCs (PMN-MDSCs). Indole-3-propionic acid (IPA), a natural AhR ligand produced from dietary tryptophan, significantly promoted PMN-MDSC differentiation and suppressive function on CD4

Indexed as

Myeloid-Derived Suppressor CellsSjogren's SyndromeAnimalsHumansMiceMyeloid CellsReceptors, Aryl HydrocarbonT-LymphocytesReceptors, Aryl HydrocarbonAryl hydrocarbon receptormyeloid-derived suppressor cellSjogren’s syndrome

Identifiers

PMID36369368
PMCPMC9709038
OpenAlexW4308891944

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.