Evidence map›Paper›PMID 32021149›Full record

ReviewInternational journal of chronic obstructive pulmonary disease2020

How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?

Tegeleqi Bu, Li Fang Wang, Yi Qing Yin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of chronic obstructive pulmonary disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-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

38 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Identification ofFrontiers in immunology · 2026
    Review
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  5. A Combined Bioinformatics and Clinical Validation Study IdentifiesInternational journal of molecular sciences · 2025
    Article
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  7. Review
  8. Review
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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

3 authors at 1 institution in 1 country.

Tegeleqi BuDepartment of Anesthesiology, China-Japan Friendship Hospital, Beijing, People's Republic of China.ORCID 0000-0002-4771-6052
Li Fang WangDepartment of Anesthesiology, China-Japan Friendship Hospital, Beijing, People's Republic of China.
Yi Qing YinDepartment of Anesthesiology, China-Japan Friendship Hospital, Beijing, People's Republic of China.
China-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the therapeutic potential of immune-modulation during the progression of chronic obstructive pulmonary disease (COPD) has been attracting increasing interest. However, chronic inflammatory response has been over-simplified in descriptions of the mechanism of COPD progression. As a form of first-line airway defense, epithelial cells exhibit phenotypic alteration, and participate in epithelial layer disorganization, mucus hypersecretion, and extracellular matrix deposition. Dendritic cells (DCs) exhibit attenuated antigen-presenting capacity in patients with advanced COPD. Immature DCs migrate into small airways, where they promote a pro-inflammatory microenvironment and bacterial colonization. In response to damage-associated molecular patterns (DAMPs) in lung tissue affected by COPD, neutrophils are excessively recruited and activated, where they promote a proteolytic microenvironment and fibrotic repair in small airways. Macrophages exhibit decreased phagocytosis in the large airways, while they demonstrate high pro-inflammatory potential in the small airways, and mediate alveolar destruction and chronic airway inflammation. Natural killer T (NKT) cells, eosinophils, and mast cells also play supplementary roles in COPD progression; however, their cellular activities are not yet entirely clear. Overall, during COPD progression, "exhausted" innate immune responses can be observed in the large airways. On the other hand, the innate immune response is enhanced in the small airways. Approaches that inhibit the inflammatory cascade, chemotaxis, or the activation of inflammatory cells could possibly delay the progression of airway remodeling in COPD, and may thus have potential clinical significance.

Indexed as

Airway RemodelingImmunity, CellularImmunity, InnateAnimalsDendritic CellsDisease ProgressionEosinophilsHumansLungMacrophagesMast CellsNatural Killer T-CellsNeutrophilsPulmonary Disease, Chronic ObstructiveSignal Transductionairway remodelingchronic obstructive pulmonary diseaseimmune toleranceinnate immune celllung immunity

Identifiers

PMID32021149
PMCPMC6966950
OpenAlexW2999850455

What OpenQuestion holds

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LicenceCC BY-NC
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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.