Evidence map›Paper›PMID 27236363›Full record

ReviewTrends in immunology2016

Regulation of the T Cell Response by CD39.

Maisa C Takenaka, Simon Robson, Francisco J Quintana

Open access · greenAbstract readReview
In one paragraph

Review in Trends in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
14.5field-weighted citation impact, top 1% 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

130 citing papers in PubMed, 195 citations in OpenAlex.

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  11. Metabolism of myeloid cells in brain tumors.Frontiers in immunology · 2026
    Review
  12. Efferocytosis-associated Mrc1Frontiers in immunology · 2026
    Article
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70 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

Maisa C TakenakaAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Simon RobsonDivisions of Gastroenterology, Hepatology, and Transplantation, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: srobson@bidmc.harvard.edu.
Francisco J QuintanaAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard, Cambridge, MA, USA. Electronic address: fquintana@rics.bwh.harvard.edu.
Beth Israel Deaconess Medical Center · USBrigham and Women's Hospital · USBroad Institute · US

Funding

XENOGRAFT TOLERANCE THROUGH MIXED CHIMERISMP01AI045897 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Megan Sykes · 2000 to 2026
$71.9M
Role of AHR in Dendritic Cells in the Control of the CNS AutoimmunityR01ES025530 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI Francisco J. Quintana · 2016 to 2026
$3.7M
Regulation of CNS AutoimmunityR01AI126880 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI QUINTANA, FRANCISCO J. · 2017 to 2021
$2.1M
Purinergic ThromboregulationR01HL094400 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2009 to 2010
$1.4M
Engineering Inhibitory Antibodies to Ectoenzymes for Cancer TreatmentR21CA164970 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2012 to 2013
$405k
NCI NIH HHS R21 CA164970NHLBI NIH HHS R01 HL094400NIAID NIH HHS P01 AI045897NIAID NIH HHS R01 AI126880NIEHS NIH HHS R01 ES025530
6 · The paper itself

Abstract

The ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1, or CD39) catalyzes the phosphohydrolysis of extracellular ATP (eATP) and ADP (eADP) released under conditions of inflammatory stress and cell injury. CD39 generates AMP, which is in turn used by the ecto-5'-nucleotidase CD73 to synthesize adenosine. These ectonucleotidases have a major impact on the dynamic equilibrium of proinflammatory eATP and ADP nucleotides versus immunosuppressive adenosine nucleosides. Indeed, CD39 plays a dominant role in the purinergic regulation of inflammation and the immune response because its expression is influenced by genetic and environmental factors. We review the specific role of CD39 in the kinetic regulation of cellular immune responses in the evolution of disease. We focus on the effects of CD39 on T cells and explore potential clinical applications in autoimmunity, chronic infections, and cancer.

Indexed as

5'-NucleotidaseAdenosineAdenosine MonophosphateAnimalsAntigens, CDApyraseAutoimmune DiseasesAutoimmunityGene-Environment InteractionHumansImmune ToleranceInfectionsInflammationLymphocyte ActivationNeoplasmsT-Lymphocytes5'-NucleotidaseAdenosineAdenosine MonophosphateAntigens, CDApyraseCD39 antigen

Identifiers

PMID27236363
PMCPMC5215082
OpenAlexW2396424530

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.