Evidence map›Paper›PMID 39435598›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

CD169+ Macrophages Mediate the Immune Response of Allergic Rhinitis Through the Keap1/Nrf2/HO-1 Axis.

Wenwen Qi, Chengcheng Liu, Lei Shi, Hui Li, Xiaozhi Hou, Hongjie Du, Luqiu Chen, Xiaochen Gao, Xue Cao, Na Guo and 10 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Bone marrow-derived CD169Experimental & molecular medicine · 2025
    Article
  10. Article
  11. Article
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

20 authors.

Wenwen QiDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Chengcheng LiuDepartment of Central Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Lei ShiDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Hui LiDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Xiaozhi HouDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Hongjie DuDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Luqiu ChenDepartment of Pediatric Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.
Xiaochen GaoDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Xue CaoDepartment of Otolaryngology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Na GuoDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Yuhan DongDepartment of Otolaryngology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Chengzhilin LiDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Fanyu YuanDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Zhenxiao TengDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Houyang HuDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Fangyuan ZhuDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Xuanchen ZhouDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Lulu GuoAdvanced Medical Research Institute, Cheeloo College of Medicine, NHC Key Laboratory of Otorhinolaryngology, Shandong University, Jinan, China.
Miaoqing ZhaoDepartment of Pathology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China.
Ming XiaDepartment of Otolaryngology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID 0000-0002-3735-5468

Funding

China Postdoctoral Science Foundation 2024M751886National Natural Science Foundation of China #82071013National Natural Science Foundation of China #82071035National Natural Science Foundation of China #82371118National Natural Science Foundation of China #82371165National Natural Science Foundation of China #82401329National Natural Science Foundation of China-Shandong Joint Fund for Marine Science Research Centers ZR2021LSW028National Natural Science Foundation of China-Shandong Joint Fund for Marine Science Research Centers ZR2022LZL001Natural Science Foundation of Shandong Province ZR2023MH106Natural Science Foundation of Shandong Province ZR2023MH364Taishan Scholar Foundation of Shandong Province tsqn201812134
6 · The paper itself

Abstract

CD169+ macrophages are a newly defined macrophage subpopulation that can recognize and bind with other cells through related ligands, playing an essential role in antigen presentation and immune tolerance. However, its role in Allergic Rhinitis (AR) is still unclear. To investigate the characteristics of CD169+ macrophages in AR, this work first detects their expression patterns in the nasal mucosa of clinical patients. These results show a significant increase in CD169+ macrophages in the nasal mucosa of patients with AR. Subsequently, this work establishes an animal AR model using CD169 transgenic mice and compared the advantages of the two models. Moreover, this work also demonstrates the effects of CD169 knockout on eosinophils, Th cells, Treg cells, and the migration of dendritic cells (DCs). In addition, this metabolomic data shows that CD169+ macrophages can upregulate alanine production and increase reactive oxygen species (ROS) levels. This process may be mediated through the Keap1/Nrf2/HO-1 signaling pathway. In addition, this work also finds that SLC38A2 plays an essential role in the process of CD169+ macrophages promoting alanine uptake by DCs. This study confirms that CD169+ macrophages can upregulate their internal alanine production and increase ROS levels through the Keap1/Nrf2/HO-1 axis, playing an irreplaceable role in AR.

Indexed as

Disease Models, AnimalHeme Oxygenase-1Kelch-Like ECH-Associated Protein 1MacrophagesMice, TransgenicNF-E2-Related Factor 2Rhinitis, AllergicSialic Acid Binding Ig-like Lectin 1Signal TransductionAnimalsFemaleHumansMaleMiceHeme Oxygenase-1Kelch-Like ECH-Associated Protein 1Nfe2l2 protein, mouseNF-E2-Related Factor 2Sialic Acid Binding Ig-like Lectin 1allergic rhinitisCD169+ macrophagesimmune responseKeap1/Nrf2/HO‐1 axisROS

Identifiers

PMID39435598
PMCPMC11615775

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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.