Evidence map›Paper›PMID 23520507›Full record

ArticlePloS one2013

Graft-versus-host disease is enhanced by selective CD73 blockade in mice.

Long Wang, Jie Fan, Siqi Chen, Yi Zhang, Tyler J Curiel, Bin Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. 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
3.2field-weighted citation impact, top 9% 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, 45 citations in OpenAlex.

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  14. Human Mesenchymal Stem Cell-Educated Macrophages Are a Distinct High IL-6-Producing Subset that Confer Protection in Graft-versus-Host-Disease and Radiation Injury Models.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2017
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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

6 authors at 4 institutions in 2 countries.

Long WangDepartment of Medicine, University of Texas Health Science Center, San Antonio, Texas, United States of America.
Jie Fan
Siqi Chen
Yi Zhang
Tyler J Curiel
Bin Zhang
The University of Texas Health Science Center at San Antonio · USFirst Affiliated Hospital of Zhengzhou University · CNNorthwestern University · USRobert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robin Jean Leach · 1991 to 2026
$59.1M
INSTITUTE FOR INTEGRATION OF MEDICINE & SCIENCE: A PARTNERSHIP TO IMPROVE HEALTHUL1RR025767 · NCRR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2008 to 2011
$23.8M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR000149 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A · 2012 to 2013
$6.8M
CD73 and Tumor Immunity-CD73 and CTLA-4 combination Blockade in Ovarian CancerR01CA149669 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZHANG, BIN · 2011 to 2015
$1.7M
NCATS NIH HHS UL1 TR000149NCATS NIH HHS UL1 TR001120NCI NIH HHS 2P30 CA054174-17NCI NIH HHS CA149669NCI NIH HHS P30 CA054174NCI NIH HHS R01 CA149669NCRR NIH HHS UL1 RR025767NCRR NIH HHS UL1RR025767
6 · The paper itself

Abstract

CD73 functions as an ecto-5'-nucleotidase to produce extracellular adenosine that has anti-inflammatory and immunosuppressive activity. We here demonstrate that CD73 helps control graft-versus-host disease (GVHD) in mouse models. Survival of wild-type (WT) recipients of either allogeneic donor naïve CD73 knock-out (KO) or WT T cells was similar suggesting that donor naïve T cell CD73 did not contribute to GVHD. By contrast, donor CD73 KO CD4(+)CD25(+) regulatory T cells (Treg) had significantly impaired ability to mitigate GVHD mortality compared to WT Treg, suggesting that CD73 on Treg is critical for GVHD protection. However, compared to donor CD73, recipient CD73 is more effective in limiting GVHD. Pharmacological blockade of A2A receptor exacerbated GVHD in WT recipients, but not in CD73 KO recipients, suggesting that A2 receptor signaling is primarily implicated in CD73-mediated GVHD protection. Moreover, pharmacological blockade of CD73 enzymatic activity induced stronger alloreactive T cell activity, worsened GVHD and enhanced the graft-versus-leukemia (GVL) effect. These findings suggest that both donor and recipient CD73 protects against GVHD but also limits GVL effects. Thus, either enhancing or blocking CD73 activity has great potential clinical application in allogeneic bone marrow transplants.

Indexed as

Bone Marrow Transplantation5'-NucleotidaseAdenosine A2 Receptor AntagonistsAnimalsGraft vs Host DiseaseGraft vs Leukemia EffectMiceMice, Inbred BALB CMice, KnockoutReceptor, Adenosine A2AT-Lymphocytes, RegulatoryTransplantation, Homologous5'-NucleotidaseAdenosine A2 Receptor AntagonistsReceptor, Adenosine A2A

Identifiers

PMID23520507
PMCPMC3592842
OpenAlexW2061448307

What OpenQuestion holds

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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.