Evidence map›Paper›PMID 29676596›Full record

ArticleAmerican journal of respiratory and critical care medicine2018

Lung Dendritic Cells Drive Natural Killer Cytotoxicity in Chronic Obstructive Pulmonary Disease via IL-15Rα.

Donna K Finch, Valerie R Stolberg, John Ferguson, Henrih Alikaj, Mohamed R Kady, Bradley W Richmond, Vasiliy V Polosukhin, Timothy S Blackwell, Lisa McCloskey, Jeffrey L Curtis and 1 more

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03034642 (Modulation of Steroid Immunosuppression by Alveolar Efferocytosis), which is not on this map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.0field-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.

NCT03034642 nacompletednot on this map

Modulation of Steroid Immunosuppression by Alveolar Efferocytosis

TypeinterventionalSponsorVA Ann Arbor Healthcare SystemRan2015 to 2021Enrolled60ConditionsPulmonary Disease, Chronic Obstructive, Pneumonia, BacterialArmsBronchoscopy with bilateral bronchoalveolar lavages
3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Predominant lung cDC2 phenotype in cigarette smoke-exposed mice favors polarization of IL-17-producing CD4American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
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  7. Single-cell hdWGCNA reveals a novel diagnostic model and signature genes of macrophages associated with chronic obstructive pulmonary disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  8. Review
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  17. Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 2 countries.

Donna K Finch1 Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom.
Valerie R Stolberg2 Research Service, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, Michigan.
John Ferguson1 Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom.
Henrih Alikaj2 Research Service, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, Michigan.
Mohamed R Kady2 Research Service, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, Michigan.
Bradley W Richmond3 Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine.
Vasiliy V Polosukhin3 Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine.
Timothy S Blackwell3 Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine.
Lisa McCloskey7 Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan.
Jeffrey L Curtis7 Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan Health System, Ann Arbor, Michigan.
Christine M Freeman2 Research Service, Veterans Affairs Ann Arbor Healthcare System, Ann Arbor, Michigan.
VA Ann Arbor Healthcare System · USInstitute of Neuroimmunology of the Slovak Academy of Sciences · SKPulmonary and Allergy Associates · USUniversity of Michigan · USMichigan Medicine · USVanderbilt University · US

Funding

Role of p73 in COPD PathogenesisK08HL138088 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHMOND, BRADLEY WINSTON · 2017 to 2018
$317k
Mechanisms driving airway inflammation in chronic lung diseaseI01BX002378 · VA · VETERANS HEALTH ADMINISTRATION · PI Timothy S. Blackwell · 2014 to 2026
–
Modulation of Steroid Suppression by Alveolar Macrophage EfferocytosisI01CX000911 · VA · VETERANS HEALTH ADMINISTRATION · PI CURTIS, JEFFREY LOUIS · 2016 to 2020
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Regulatory T Cell Inhibition of Natural Killer Cells in COPDI01CX001553 · VA · VETERANS HEALTH ADMINISTRATION · PI Christine M Basmajian · 2017 to 2026
–
BLRD VA I01 BX002378CSRD VA I01 CX000911CSRD VA I01 CX001553NHLBI NIH HHS K08 HL138088
6 · The paper itself

Abstract

rationaleLung natural killer cells (NKs) kill a greater percentage of autologous lung parenchymal cells in chronic obstructive pulmonary disease (COPD) than in nonobstructed smokers. To become cytotoxic, NKs require priming, typically by dendritic cells (DCs), but whether priming occurs in the lungs in COPD is unknown.

methodsWe used lung tissue and in some cases peripheral blood from patients undergoing clinically indicated resections to determine in vitro killing of CD326

resultsHuman lung NKs killed isolated autologous lung epithelial cells; cytotoxicity was increased (P = 0.0001) in COPD, relative to smokers without obstruction. Similarly, increased lung NK cytotoxicity compared with control subjects was observed in CS-exposed mice and pIgR

conclusionsHeightened NK cytotoxicity against lung epithelial cells in COPD results primarily from lung DC-mediated priming via IL-15 trans-presentation on IL-15Rα. Future studies are required to test whether increased NK cytotoxicity contributes to COPD pathogenesis.

Indexed as

AgedAnimalsCigarette SmokingCytotoxinsDendritic CellsDisease Models, AnimalEpithelial CellsFemaleFlow CytometryHumansInterleukin-15 Receptor alpha SubunitIn Vitro TechniquesKiller Cells, NaturalLymphocyte ActivationMaleMiceCytotoxinsInterleukin-15 Receptor alpha Subunitchronic obstructive pulmonary diseasecigarette smokehumansmall-airway epithelial cells

Identifiers

PMID29676596
PMCPMC6221577
OpenAlexW2800567595

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.