Evidence map›Paper›PMID 18073395›Full record

ReviewProceedings of the American Thoracic Society2007

Toll-like receptors, Notch ligands, and cytokines drive the chronicity of lung inflammation.

Tracy Raymond, Matthew Schaller, Cory M Hogaboam, Nicholas W Lukacs, Rosemary Rochford, Steven L Kunkel

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Notch signaling regulates pulmonary fibrosis.Frontiers in cell and developmental biology · 2024
    Review
  2. Article
  3. Review
  4. Article
  5. Regulation of Notch 1 signaling in THP-1 cells enhances M2 macrophage differentiation.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Delta-like 1-Lysine613 regulates notch signaling.Biochimica et biophysica acta · 2011
    Article
  11. Toll like receptors in diseases of the lung.International immunopharmacology · 2011
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Canonical and non-canonical Notch ligands.Current topics in developmental biology · 2010
    Review
  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

6 authors at 2 institutions in 1 country.

Tracy RaymondImmunology Program and Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109-2200, USA.
Matthew Schaller
Cory M Hogaboam
Nicholas W Lukacs
Rosemary Rochford
Steven L Kunkel
University of Michigan · USSUNY Upstate Medical University · US

Funding

MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1985 to 2009
$14.1M
SCCOR in Translational Research in Acute Lung InjuryP50HL074024 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HYZY, ROBERT C · 2003 to 2007
$13.5M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
MONOKINE GENE EXPRESSION/REGULATION IN LUNG INJURYR01HL031237 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KUNKEL, STEVEN LYNN, STANDIFORD, THEODORE J. · 1985 to 2017
$5.9M
NHLBI NIH HHS HL31237NHLBI NIH HHS HL31963NHLBI NIH HHS HL74024NIAID NIH HHS T32 AI007413
6 · The paper itself

Abstract

Current dogma supports the concept that the expression of a disease-inducing signature cytokine phenotype is important to the maintenance stage of chronic lung disorders. This cytokine phenotype has been characterized as a polarization toward type 2 cytokines, which are profibrotic and immunoregulatory. The biology of this latter activity could mechanistically explain pathogen-induced exacerbation of chronic lung inflammation, as a skewed cytokine profile in the lung alters dendritic cell function, activates fibroblasts, and facilitates a subsequent "second hit" by an infectious pathogen. In this setting, cytokine biology is also linked to Toll-like receptors (TLRs) in the maintenance of lung immunity, as the activity of this receptor-ligand system by both leukocytes and stromal cells is likely an important component of disease chronicity. The participation of dendritic cells via TLRs in chronic lung disease could facilitate communication circuits established between antigen-presenting cells and lymphocytes. Data suggest that TLR activation via myeloid differentiation factor 88 adaptor protein leads to the induction of a Notch ligand known as Delta-like-4 on dendritic cells that activate the Notch receptor on T cells, promoting a helper T-cell type 1 cytokine response. It is likely that the evolution of host defense signals designed to recognize patterns emitted from a hostile microbial environment may now be superimposed on adaptive immunity and provide the underpinning to support the maintenance of chronic lung disease.

Indexed as

AnimalsCytokinesDendritic CellsDisease Models, AnimalInflammationLung DiseasesMacrophagesPhenotypeToll-Like ReceptorsVirus DiseasesCytokinesToll-Like Receptors

Identifiers

PMID18073395
PMCPMC2647651
OpenAlexW2107286110

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.