Evidence map›Paper›PMID 16322591›Full record

ReviewProceedings of the American Thoracic Society2005

Cell-mediated adaptive immune defense of the lungs.

Jeffrey L Curtis

Registry-linked trialOpen access · greenAbstract readComparative StudyReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00281229 (Innate and Adaptive Immunity in COPD Exacerbations), which is not on this map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-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.

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

28 citing papers in PubMed, 79 citations in OpenAlex.

  1. Nanoparticle-Based Pulmonary Immune Engineering.Annual review of chemical and biomolecular engineering · 2025
    Review
  2. Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025
    Review
  3. Review
  4. Aerosol pulmonary immune engineering.Advanced drug delivery reviews · 2023
    Review
  5. Review
  6. Spinal Cord Injury Impairs Lung Immunity in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Bronchiectasis in COPD-OSA Overlap Syndrome Patients.International journal of chronic obstructive pulmonary disease · 2020
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. ATS Core Curriculum 2016: Part III. Pediatric Pulmonary Medicine.Annals of the American Thoracic Society · 2016
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

1 author at 1 institution in 2 countries.

Jeffrey L CurtisPulmonary and Critical Care Medicine Section (506/111G), Department of Veterans Affairs Health System, 2215 Fuller Road, Ann Arbor, MI 48105-2303, USA. jlcurtis@umich.edu
VA Ann Arbor Healthcare System · US

Funding

PULMONARY LYMPHOCYTE APOPTOSIS AND CELL CYCLE ARRESTR01HL056309 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CURTIS, JEFFREY LOUIS · 1996 to 2010
$2.5M
NHLBI NIH HHS R01 HL056309
6 · The paper itself

Abstract

Cell-mediated adaptive immune responses contribute to defense against all classes of pulmonary pathogens and are essential against viruses, mycobacteria, and fungi, including Pneumocystis carinii. Adaptive responses depend on sequential pairwise interactions between three cell types: T cells, natural killer (NK) cells, and dendritic cells (DC). Differential expression of specific adhesion molecules and chemokines regulates the location and timing of these interactions. Primary adaptive responses are triggered by immature myeloid DC, which carry antigen from the lungs to regional lymph nodes. Antigen presentation by these mature DC is required to activate naive CD4 T cells, which are essential to generate polarized type 1 or type 2 effector responses and for robust immunologic memory. Inflammation recruits NK cells and DC that interact in a contact- and tumor necrosis factor-alpha-dependent fashion within injured tissues to initiate immune response polarization. NK cells exposed to IL-12 favor survival of DC that prime for Th1 responses, whereas NK cells exposed to IL-4 do not exert DC selection, leading to tolerogenic or Th2 responses. Naive alphabeta T cells, NK cells, and DC also amplify secondary adaptive responses to previously encountered pathogens. However, secondary responses are accelerated because memory T cells can migrate directly to infected tissues where they can be activated without strenuous costimulatory requirements. Additionally, previous pulmonary infections or immune responses increase numbers of lung DC and populate the lungs with clones of memory B cells and T cells that are immediately available to respond to infections.

Indexed as

Adaptation, PhysiologicalCell CommunicationDendritic CellsHumansImmunity, CellularImmunocompetenceKiller Cells, NaturalPneumoniaRisk AssessmentSensitivity and SpecificityT-Lymphocytes

Identifiers

PMID16322591
PMCPMC2259246
OpenAlexW2146644563

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.