Evidence map›Paper›PMID 15725351›Full record

ArticleRespiratory research2005

CXCR3/CXCL10 interactions in the development of hypersensitivity pneumonitis.

Carlo Agostini, Fiorella Calabrese, Venerino Poletti, Guido Marcer, Monica Facco, Marta Miorin, Anna Cabrelle, Ilenia Baesso, Renato Zambello, Livio Trentin and 1 more

Open access · goldAbstract readControlled Clinical Trial
In one paragraph

Article in Respiratory research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Circulating Plasma Biomarkers of Progressive Interstitial Lung Disease.American journal of respiratory and critical care medicine · 2020
    Article
  7. Cytokine gene polymorphisms in Pigeon Breeder's Disease expression.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. 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

11 authors at 2 institutions in 1 country.

Carlo AgostiniPadua University School of Medicine, Department of Clinical and Experimental Medicine, Clinical Immunology Branch, via Giustiniani 2, 35128 Padua, Italy. carlo.agostini@unipd.it
Fiorella Calabrese
Venerino Poletti
Guido Marcer
Monica Facco
Marta Miorin
Anna Cabrelle
Ilenia Baesso
Renato Zambello
Livio Trentin
Gianpietro Semenzato
University of Padua · ITCarlo Forlanini Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypersensitivity pneumonitis (HP) is an interstitial lung disease caused by repeated inhalations of finely dispersed organic particles or low molecular weight chemicals. The disease is characterized by an alveolitis sustained by CD8(+) cytotoxic T lymphocytes, granuloma formation, and, whenever antigenic exposition continues, fibrosis. Although it is known that T-cell migration into the lungs is crucial in HP reaction, mechanisms implicated in this process remain undefined.

methodsUsing flow cytometry, immunohistochemistry, confocal microscopy analysis and chemotaxis assays we evaluated whether CXCL10 and its receptor CXCR3 regulate the trafficking of CD8(+) T cells in HP lung.

resultsOur data demonstrated that lymphocytes infiltrating lung biopsies are CD8 T cells which strongly stain for CXCR3. However, T cells accumulating in the BAL of HP were CXCR3(+)/IFNgamma(+) Tc1 cells exhibiting a strong in vitro migratory capability in response to CXCL10. Alveolar macrophages expressed and secreted, in response to IFN-gamma, definite levels of CXCL10 capable of inducing chemotaxis of the CXCR3(+) T-cell line. Interestingly, striking levels of CXCR3 ligands could be demonstrated in the fluid component of the BAL in individuals with HP.

conclusionThese data indicate that IFN-gamma mediates the recruitment of lymphocytes into the lung via production of the chemokine CXCL10, resulting in Tc1-cell alveolitis and granuloma formation.

Indexed as

AdultAlveolitis, Extrinsic AllergicCD8-Positive T-LymphocytesCell MovementChemokine CXCL10Chemokines, CXCFemaleHumansInterferon-gammaLymphocyte ActivationMaleReceptors, ChemokineReceptors, CXCR3Chemokine CXCL10Chemokines, CXCCXCL10 protein, humanCXCR3 protein, humanInterferon-gammaReceptors, ChemokineReceptors, CXCR3

Identifiers

PMID15725351
PMCPMC554979
OpenAlexW1515753814

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.