Evidence map›Paper›PMID 23374856›Full record

Trial reportRespiratory research2013

Lung CD8+ T cells in COPD have increased expression of bacterial TLRs.

Christine M Freeman, Fernando J Martinez, Meilan K Han, George R Washko, Alexandra L McCubbrey, Stephen W Chensue, Douglas A Arenberg, Catherine A Meldrum, Lisa McCloskey, Jeffrey L Curtis

2 registry-linked trialsOpen access · goldAbstract readClinical Trial
In one paragraph

Trial report in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
13.7field-weighted citation impact, top 1% 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.

NCT00281216 completednot on this map

Innate and Adaptive Immunity in COPD Exacerbations: Prospective Cohort Study

TypeobservationalSponsorUniversity of MichiganRan2005 to 2010Enrolled10ConditionsPulmonary Disease, Chronic Obstructive, Lung Diseases, Lung Diseases, Obstructive
NCT00281229 completednot on this map

Innate and Adaptive Immunity in COPD Exacerbations: Surgical Volunteers

TypeobservationalSponsorUniversity of MichiganRan2005 to 2015Enrolled481ConditionsPulmonary Disease, Chronic Obstructive, Lung Diseases, Obstructive
3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).Journal of toxicology and environmental health. Part B, Critical reviews · 2023
    Review
  4. Effects of Inhaled Corticosteroids on the Innate Immunological Response toInternational journal of molecular sciences · 2022
    Article
  5. Mechanisms of immune regulation for acupuncture on chronic respiratory diseases.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Can SARS-CoV-2 Virus Use Multiple Receptors to Enter Host Cells?International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. The Role of Toll-Like Receptors 2 and 4 in the Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2020
    Review
  15. COPD as a Disease of Immunosenescence.Yonsei medical journal · 2019
    Review
  16. Article
  17. Multitissue Transcriptomics Delineates the Diversity of Airway T Cell Functions in Asthma.American journal of respiratory cell and molecular biology · 2018
    Article
  18. Review
  19. Review
  20. Th17 profile in COPD exacerbations.International journal of chronic obstructive pulmonary disease · 2017
    Review
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

10 authors at 4 institutions in 1 country.

Christine M FreemanResearch Service, Department of Veterans Affairs Healthcare System, Ann Arbor, MI 48105, USA. cmfreema@med.umich.edu
Fernando J Martinez
Meilan K Han
George R Washko
Alexandra L McCubbrey
Stephen W Chensue
Douglas A Arenberg
Catherine A Meldrum
Lisa McCloskey
Jeffrey L Curtis
Michigan Medicine · USHarvard University · USUniversity of Michigan–Ann Arbor · USVA Ann Arbor Healthcare System · US

Funding

RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Innate and adaptive immunity in COPD exacerbationsR01HL082480 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CURTIS, JEFFREY LOUIS · 2005 to 2009
$2.4M
PREDICTING RESPONSE TO THERAPY IN IDIOPATHIC PULMONARY FK24HL004212 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARTINEZ, FERNANDO J · 2000 to 2009
$1.2M
Impact of Gender on Symptoms and Progression of IPFK23HL093351 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HAN, MEILAN K · 2009 to 2013
$553k
NCI NIH HHS P30 CA46952NHLBI NIH HHS K23 HL093351NHLBI NIH HHS K24 HL04212NIAID NIH HHS T32 AI007413
6 · The paper itself

Abstract

backgroundToll-like receptors (TLRs) on T cells can modulate their responses, however, the extent and significance of TLR expression by lung T cells, NK cells, or NKT cells in chronic obstructive pulmonary disease (COPD) is unknown.

methodsLung tissue collected from clinically-indicated resections (n = 34) was used either: (a) to compare the expression of TLR1, TLR2, TLR2/1, TLR3, TLR4, TLR5, TLR6 and TLR9 on lung CD8+ T cells, CD4+ T cells, NK cells and NKT cells from smokers with or without COPD; or (b) to isolate CD8+ T cells for culture with anti-CD3ε without or with various TLR ligands. We measured protein expression of IFN-γ, TNF-α, IL-13, perforin, granzyme A, granzyme B, soluble FasL, CCL2, CCL3, CCL4, CCL5, CCL11, and CXCL9 in supernatants.

resultsAll the lung subsets analyzed demonstrated low levels of specific TLR expression, but the percentage of CD8+ T cells expressing TLR1, TLR2, TLR4, TLR6 and TLR2/1 was significantly increased in COPD subjects relative to those without COPD. In contrast, from the same subjects, only TLR2/1 and TLR2 on lung CD4+ T cells and CD8+ NKT cells, respectively, showed a significant increase in COPD and there was no difference in TLR expression on lung CD56+ NK cells. Production of the Tc1 cytokines IFN-γ and TNF-α by lung CD8+ T cells were significantly increased via co-stimulation by Pam3CSK4, a specific TLR2/1 ligand, but not by other agonists. Furthermore, this increase in cytokine production was specific to lung CD8+ T cells from patients with COPD as compared to lung CD8+ T cells from smokers without COPD.

conclusionsThese data suggest that as lung function worsens in COPD, the auto-aggressive behavior of lung CD8+ T cells could increase in response to microbial TLR ligands, specifically ligands against TLR2/1.

Indexed as

Gene Expression Regulation, BacterialAgedCD8-Positive T-LymphocytesCells, CulturedFemaleHumansLungMaleMiddle AgedProspective StudiesPulmonary Disease, Chronic ObstructiveToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID23374856
PMCPMC3583694
OpenAlexW2168733379

What OpenQuestion holds

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LicenceCC BY
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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.