Evidence map›Paper›PMID 26595735›Full record

ReviewAnnals of the American Thoracic Society2015

Immune Dysfunction in Patients with Chronic Obstructive Pulmonary Disease.

Tariq A Bhat, Louis Panzica, Suresh Gopi Kalathil, Yasmin Thanavala

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the American Thoracic Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 3 pooled it
6.0field-weighted citation impact, top 3% 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

148 citing papers in PubMed, 3 syntheses or guidelines pooled it, 214 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Risk Factors for Secondary Immunodeficiency in the Aged.The journal of allergy and clinical immunology. In practice · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Airway Goblet Metaplasia Resulting from YAP/TAZ Deletion Drives Pulmonary Inflammatory Responses.American journal of respiratory cell and molecular biology · 2026
    Article
  16. Observational
  17. Review
  18. Article
  19. Review
  20. Article

88 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

4 authors at 1 institution in 1 country.

Tariq A BhatDepartment of Immunology, Roswell Park Cancer Institute, Buffalo, New York.
Louis PanzicaDepartment of Immunology, Roswell Park Cancer Institute, Buffalo, New York.
Suresh Gopi KalathilDepartment of Immunology, Roswell Park Cancer Institute, Buffalo, New York.
Yasmin ThanavalaDepartment of Immunology, Roswell Park Cancer Institute, Buffalo, New York.
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
Innate and adaptive immune response to bacterial infections in COPD patientsR56AI069379 · NIAID · ROSWELL PARK CANCER INSTITUTE CORP · PI THANAVALA, YASMIN · 2008 to 2009
$890k
NCI NIH HHS P30 CA016056NIAID NIH HHS AI069379NIAID NIH HHS R56 AI069379
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a complex chronic disease. Chronic inflammation is the hallmark of COPD, involving the interplay of a wide variety of cells in the lung microenvironment. Cigarette smoke (CS) induces chronic lung inflammation and is considered a key etiological factor in the development and pathogenesis of COPD. Structural and inflammatory cells in the lung respond to CS exposure by releasing proinflammatory mediators that recruit additional inflammatory immune cells, which collectively contribute to the establishment of a chronic inflammatory microenvironment. Chronic inflammation contributes to lung damage, compromises innate and adaptive immune responses, and facilitates the recurrent episodes of respiratory infection that punctuate and further contribute to the pathological manifestations of the stable disease. A number of studies support the conclusion that immune dysfunction leads to exacerbations and disease severity in COPD. Our group has clearly demonstrated that CS exacerbates lung inflammation and compromises immunity to respiratory pathogens in a mouse model of COPD. We have also investigated the phenotype of immune cells in patients with COPD compared with healthy control subjects and found extensive immune dysfunction due to the presence and functional activity of T regulatory cells, CD4(+)PD-1(+) exhausted effector T cells and myeloid-derived suppressor cells. Manipulation of these immunosuppressive networks in COPD could provide a rational strategy to restore functional immune responses, reduce exacerbations, and improve lung function. In this review, we discuss the role of immune dysfunction in COPD that may contribute to recurrent respiratory infections and disease severity.

Indexed as

Adaptive ImmunityAnimalsDisease Models, AnimalDisease ProgressionHumansImmunity, InnateInflammationMicePulmonary Disease, Chronic ObstructiveSmokingT-Lymphocytes, Regulatoryadaptive immunityCOPDimmune dysfunctioninnate immunity

Identifiers

PMID26595735
PMCPMC4722840
OpenAlexW2179187436

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.