Evidence map›Paper›PMID 19934352›Full record

ReviewProceedings of the American Thoracic Society2009

The aging immune system and its relationship to the development of chronic obstructive pulmonary disease.

Gulshan Sharma, Nicola A Hanania, Y Michael Shim

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Global herpes zoster burden in adults with COPD: a systematic review and meta-analysis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Pooled it
  2. Review
  3. Article
  4. Predictive Value of Biological Age for All-Cause Mortality in Patients with COPD.International journal of chronic obstructive pulmonary disease · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Effect of physical activity in lymphocytes senescence burden in patients with COPD.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Macrophages in Lung Repair and Fibrosis.Results and problems in cell differentiation · 2024
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Tumor Immunology and Immunotherapy of Non-Small-Cell Lung Cancer.Cold Spring Harbor perspectives in medicine · 2022
    Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Gulshan SharmaDivision of Pulmonary Allergy and Critical Care Medicine, University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-0561, USA. gulshan.sharma@utmb.edu
Nicola A Hanania
Y Michael Shim
Baylor College of Medicine · USThe University of Texas Medical Branch at Galveston · USUniversity of Virginia · US

Funding

Biology of Leukotrienes in the Pathogenesis of EmphysemaK08HL091127 · NHLBI · UNIVERSITY OF VIRGINIA · PI SHIM, YUN MICHAEL · 2008 to 2012
$643k
NHLBI NIH HHS K08 HL091127
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs that usually manifests late in life. Physiologic and immunologic changes that occur in COPD often mimic changes seen in the aging lung. This has led some to characterize COPD as an "accelerated aging phenotype." At the molecular level, COPD and aging share common mechanisms and are associated with significant dysregulation of the immune systems. Aging and COPD are characterized by increases in proinflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha, which are implicated in aging-related inflammatory diseases and correlate with degree of obstruction in COPD. There is an age-dependent decline in naïve T cells with oligoclonal expansion of CD8(+) CD28(null) T cells from chronic antigenic stimulation. The increase in CD8(+) CD28 (null) T regulatory cells inhibits antigen-specific CD4(+) T cell responses, leading to a decline in adaptive immune response. To compensate for the decline in the adaptive immune function there is a paradoxical up-regulation of innate immune system resulting in a proinflammatory state. The dysregulated adaptive immune system with activated innate immune responses seen with aging results in recruitment and retention of neutrophils, macrophages, and CD4(+) and CD8(+) T cells in the lungs of smokers with COPD. Once the inflammation is triggered, there is a self-perpetuating cascade of inflammation and lung parenchymal damage. This review will focus on how the aging immune system may contribute to COPD development later in life in susceptible individuals.

Indexed as

AgingHumansImmunityInterleukin-6Pulmonary Disease, Chronic ObstructiveTumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID19934352
PMCPMC5820858
OpenAlexW2158912859

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.