Evidence map›Paper›PMID 16618792›Full record

ArticleThe Journal of experimental medicine2006

Fas-positive T cells regulate the resolution of airway inflammation in a murine model of asthma.

Jiankun Tong, Hozefa S Bandulwala, Bryan S Clay, Robert A Anders, Rebecca A Shilling, Diwakar D Balachandran, Bohao Chen, Joel V Weinstock, Julian Solway, Kimm J Hamann and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 75 citations in OpenAlex.

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  12. Frontiers in immunology · 2019
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  17. Prophylactic Supplementation ofFrontiers in microbiology · 2017
    Article
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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 3 institutions in 1 country.

Jiankun TongSection of Pulmonary and Critical Care Medicine, Department of Medicine, University of Chicago, Chicago, IL 60637, USA.
Hozefa S Bandulwala
Bryan S Clay
Robert A Anders
Rebecca A Shilling
Diwakar D Balachandran
Bohao Chen
Joel V Weinstock
Julian Solway
Kimm J Hamann
Anne I Sperling
Pulmonary and Critical Care Associates · USTufts Medical Center · USUniversity of Chicago · US

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI russell z szmulewitz · 1985 to 2026
$122.1M
RESEARCH TRAINING IN RESPIRATORY BIOLOGYT32HL007605 · NHLBI · UNIVERSITY OF CHICAGO · PI Yun Fang, Gokhan M. Mutlu · 1985 to 2026
$18.1M
Molecular Mechanisms of AsthmaP01AI056352 · NIAID · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2003 to 2007
$5.6M
The role of ICOS in allergic airway diseaseR01AI050180 · NIAID · UNIVERSITY OF CHICAGO · PI SPERLING, ANNE I. · 2001 to 2005
$1.7M
Eosinophil-Airway Epithelial Fas-FasL InteractionsR01HL066026 · NHLBI · UNIVERSITY OF CHICAGO · PI HAMANN, KIMM J · 2001 to 2004
$1.3M
REGULATION OF EOSINOPHIL SURVIVALR01AI046549 · NIAID · UNIVERSITY OF CHICAGO · PI SPERLING, ANNE I. · 2000 to 2004
$1.3M
NCI NIH HHS P30 CA014599NCI NIH HHS P30-CA14599NHLBI NIH HHS R01 HL066026NHLBI NIH HHS R01 HL66026NHLBI NIH HHS T32 HL007605NHLBI NIH HHS T32 HL-07605NIAID NIH HHS P01 AI056352NIAID NIH HHS P01 AI56352NIAID NIH HHS R01 AI046549NIAID NIH HHS R01 AI050180NIAID NIH HHS R01 AI46549NIAID NIH HHS R01 AI50180
6 · The paper itself

Abstract

Persistent airway inflammation, mucus production, and airway hyperreactivity are the major contributors to the frequency and severity of asthma. Why lung inflammation persists in asthmatics remains unclear. It has been proposed that Fas-mediated apoptosis of inflammatory cells is a fundamental mechanism involved in the resolution of eosinophilic airway inflammation. Because infiltrating eosinophils are highly sensitive to Fas-mediated apoptosis, it has been presumed that direct ligation of Fas on eosinophils is involved. Here, we utilize adoptive transfers of T cells to demonstrate that the delayed resolution of eosinophilia in Fas-deficient mice is a downstream effect of Fas deficiency on T cells, not eosinophils. Interestingly, the mice that received Fas-deficient T cells, but not the controls, developed a persistent phase of inflammation that failed to resolve even 6 wk after the last challenge. This persistent phase correlated with decreased interferon (IFN)gamma production by Fas-deficient T cells and could be reproduced with adoptive transfer of IFNgamma-deficient T cells. These data demonstrate that Fas deficiency on T cells is sufficient for the development of long-term allergic airway disease in mice and implies that deregulation of death receptors such as Fas on human T cells could be an important factor in the development and/or chronic nature of asthma.

Indexed as

Adoptive TransferAnimalsAsthmaChronic DiseaseDisease Models, AnimalEosinophiliaEosinophilsfas ReceptorHumansInflammationInterferon-gammaLungMiceMice, KnockoutTime FactorsT-Lymphocytesfas ReceptorInterferon-gamma

Identifiers

PMID16618792
PMCPMC2121201
OpenAlexW2111942445

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.