Evidence map›Paper›PMID 29250768›Full record

ArticleImmunology2018

Critical involvement of atypical chemokine receptor CXCR7 in allergic airway inflammation.

Hung-Chih Chang, Po-Han Huang, Fu-Sheng Syu, Chia-Hung Hsieh, Sunny Li-Yun Chang, Jean Lu, Hui-Chen Chen

Abstract read
In one paragraph

Article in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. A novel locus for exertional dyspnoea in childhood asthma.The European respiratory journal · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Advances in CXCR7 Modulators.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  15. Article
  16. 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

7 authors.

Hung-Chih ChangGraduate Institute of Life Science, National Defence Medical Centre, Taipei, Taiwan.
Po-Han HuangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Fu-Sheng SyuGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Chia-Hung HsiehGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Sunny Li-Yun ChangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Jean LuGraduate Institute of Life Science, National Defence Medical Centre, Taipei, Taiwan.
Hui-Chen ChenGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.ORCID 0000-0001-9751-5729

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trafficking and recruitment of immune cells to the site of inflammation with spatial and temporal synchronization is crucial for the development of allergic airway inflammation. Particularly, chemokines are known to be key players in these processes. Previous studies revealed that the CXCL12/CXCR4 axis plays an important role in regulating allergic airway inflammation. However, the role of CXCR7, a recently discovered second receptor for CXCL12, in regulating airway inflammation has not been explored. Initially, CXCR7 was considered as a decoy receptor; however, numerous subsequent studies revealed that engagement of CXCR7 triggered its own signalling or modulated CXCR4-mediated signalling. In the present study, we detected the expression of CXCR7 in airway epithelial cells. Use of a lentiviral delivery system to knock down the expression of CXCR7 in the lung of sensitized mice abrogated the cardinal features of asthma, indicating that CXCR7 plays a role in regulating allergic airway inflammation. The activation of mitogen-activated protein kinase and Akt signalling in response to CXCL12 in the mouse epithelial cell line MLE-12 was reduced when CXCR7 expression was knocked down. However, either knockdown or overexpression of CXCR7 in MLE-12 did not affect CXCL12-mediated calcium influx, indicating that CXCR7 does not modulate CXCR4-mediated signalling, and that it functions as a signalling receptor rather than a decoy receptor. Finally, we found that the expression of chemokine CCL2 is regulated by CXCR7/CXCL12-mediated signalling through β-arrestin in airway epithelial cells. Hence, regulating the expression of CCL2 in airway epithelial cells may be one mechanism by which CXCR7 participates in regulating allergic airway inflammation.

Indexed as

AllergensAnimalsChemokine CCL2CytokinesDisease Models, AnimalFemaleGene ExpressionGene Knockdown TechniquesImmunoglobulin EImmunohistochemistryLungMiceReceptors, CXCRReceptors, CXCR4Respiratory HypersensitivityRespiratory MucosaAllergensChemokine CCL2Cmkor1 protein, mouseCXCR4 protein, mouseCytokinesImmunoglobulin EReceptors, CXCRReceptors, CXCR4airway epithelial cellsallergic airway inflammationCXCR7

Identifiers

PMID29250768
PMCPMC5980127

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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.