Evidence map›Paper›PMID 20083656›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

A CD1d-dependent antagonist inhibits the activation of invariant NKT cells and prevents development of allergen-induced airway hyperreactivity.

Vincent Lombardi, Philippe Stock, Abinav K Singh, Jerome Kerzerho, Wen Yang, Barbara A Sullivan, Xiangming Li, Takayuki Shiratsuchi, Nathan E Hnatiuk, Amy R Howell and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 46 citations in OpenAlex.

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  12. Lymphocyte-based model systems for allergy research: a historic overview.International archives of allergy and immunology · 2014
    Review
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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

16 authors at 7 institutions in 2 countries.

Vincent LombardiDivision of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Philippe Stock
Abinav K Singh
Jerome Kerzerho
Wen Yang
Barbara A Sullivan
Xiangming Li
Takayuki Shiratsuchi
Nathan E Hnatiuk
Amy R Howell
Karl O A Yu
Steven A Porcelli
Moriya Tsuji
Mitchell Kronenberg
S Brian Wilson
Omid Akbari
University of Southern California · USAaron Diamond AIDS Research Center · USAlbert Einstein College of Medicine · USHarvard University · USLa Jolla Institute for Immunology · USUniversity of Connecticut · USCharité - Universitätsmedizin Berlin · DE

Funding

Precision Targeting of CD1-Restricted iNKT Cells for Cancer ImmunotherapyR01AI045889 · NIAID · YESHIVA UNIVERSITY · PI Steven A Porcelli · 1999 to 2026
$9.3M
Development and Function of NKT CellsR37AI071922 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI KRONENBERG, MITCHELL · 2006 to 2015
$4.9M
Role of NKT cells in airway hyperreactivity & toleranceR01AI066020 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AKBARI, OMID · 2007 to 2011
$1.6M
NIAID NIH HHS R01 AI045889NIAID NIH HHS R01 AI066020NIAID NIH HHS R01 AI45889NIAID NIH HHS R37 AI071922NIAID NIH HHS R37 AI71922
6 · The paper itself

Abstract

The prevalence of asthma continues to increase in westernized countries, and optimal treatment remains a significant therapeutic challenge. Recently, CD1d-restricted invariant NKT (iNKT) cells were found to play a critical role in the induction of airway hyperreactivity (AHR) in animal models and are associated with asthma in humans. To test whether iNKT cell-targeted therapy could be used to treat allergen-induced airway disease, mice were sensitized with OVA and treated with di-palmitoyl-phosphatidyl-ethanolamine polyethylene glycol (DPPE-PEG), a CD1d-binding lipid antagonist. A single dose of DPPE-PEG prevented the development of AHR and pulmonary infiltration of lymphocytes upon OVA challenge, but had no effect on the development of OVA-specific Th2 responses. In addition, DPPE-PEG completely prevented the development of AHR after administration of alpha-galactosylceramide (alpha-GalCer) intranasally. Furthermore, we demonstrate that DPPE-PEG acts as antagonist to alpha-GalCer and competes with alpha-GalCer for binding to CD1d. Finally, we show that DPPE-PEG completely inhibits the alpha-GalCer-induced phosphorylation of ERK tyrosine kinase in iNKT cells, suggesting that DPPE-PEG specifically blocks TCR signaling and thus activation of iNKT cells. Because iNKT cells play a critical role in the development of AHR, the inhibition of iNKT activation by DPPE-PEG suggests a novel approach to treat iNKT cell-mediated diseases such as asthma.

Indexed as

AllergensAnimalsAntigens, CD1dBinding, CompetitiveBronchial HyperreactivityCell LineDisease Models, AnimalFemaleGalactosylceramidesHumansImmunosuppressive AgentsLymphocyte ActivationMiceMice, Inbred BALB CNatural Killer T-CellsOvalbuminAllergensalpha-galactosylceramideAntigens, CD1dCd1d1 protein, mouseCD1D protein, humanDPPE-PEG2000GalactosylceramidesImmunosuppressive AgentsOvalbuminPhosphatidylethanolaminesPolyethylene Glycols

Identifiers

PMID20083656
PMCPMC2845715
OpenAlexW1804629939

What OpenQuestion holds

Textmetadata
LicenceTDM
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.