Evidence map›Paper›PMID 33208731›Full record

ArticleNature communications2020

Endogenous antisense RNA curbs CD39 expression in Crohn's disease.

Rasika P Harshe, Anyan Xie, Marta Vuerich, Luiza Abrahão Frank, Barbora Gromova, Haohai Zhang, Rene' J Robles, Samiran Mukherjee, Eva Csizmadia, Efi Kokkotou and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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
2.1field-weighted citation impact, top 13% 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, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Peripheral CD4Frontiers in immunology · 2026
    Article
  5. Caffeine-mediated CD39Frontiers in immunology · 2026
    Article
  6. Review
  7. CD39 as a metabolic rheostat of immunoregulation.Cellular & molecular immunology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Circulation · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

15 authors at 2 institutions in 2 countries.

Rasika P HarsheDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Anyan XieDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Marta VuerichDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Luiza Abrahão FrankDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Barbora GromovaDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Haohai ZhangDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Rene' J RoblesDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Samiran MukherjeeDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Eva CsizmadiaDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Efi KokkotouDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Adam S CheifetzDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Alan C MossDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.
Satya K KotaDepartment of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA, 02115, USA.
Simon C RobsonDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA.ORCID 0000-0001-6374-0194
Maria Serena LonghiDepartment of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA, 02215, USA. mlonghi@bidmc.harvard.edu.ORCID 0000-0002-4510-1249
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

UPIT: Unleash the Potential of Intestinal TransplantationR01AI132389 · NIAID · GEORGETOWN UNIVERSITY · PI KROEMER, ALEXANDER HELMUT KURT · 2017 to 2021
$2.4M
Omics and Variable Responses to Placebo and Acupuncture in Irritable Bowel SyndroR01AT004662 · NCCIH · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAPTCHUK, TED, KOKKOTOU, EFI G. · 2009 to 2013
$2.3M
Immunomodulatory effects of bilirubin are mediated through aryl hydrocarbon receptor, O2 and purinergic pathwaysR01DK108894 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LONGHI, MARIA SERENA · 2017 to 2021
$2.0M
Engineering Inhibitory Antibodies to Ectoenzymes for Cancer TreatmentR21CA164970 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2012 to 2013
$405k
NCCIH NIH HHS R01 AT004662NCI NIH HHS R21 CA164970NIAID NIH HHS R01 AI132389NIDDK NIH HHS R01 DK108894
6 · The paper itself

Abstract

CD39 is an ectonucleotidase that initiates conversion of extracellular nucleotides into immunosuppressive adenosine. CD39 is expressed by regulatory T (Treg)-cells, where it mediates immunosuppression, and by a subset of T-helper (Th) 17-cells, where it limits pathogenicity. CD39 is regulated via single-nucleotide-polymorphisms and upon activation of aryl-hydrocarbon-receptor and oxygen-mediated pathways. Here we report a mechanism of CD39 regulation that relies on the presence of an endogenous antisense RNA, transcribed from the 3'-end of the human CD39/ENTPD1 gene. CD39-specific antisense is increased in Treg and Th17-cells of Crohn's disease patients over controls. It largely localizes in the cell nucleus and regulates CD39 by interacting with nucleolin and heterogeneous-nuclear-ribonucleoprotein-A1. Antisense silencing results in CD39 upregulation in vitro and amelioration of disease activity in a trinitro-benzene-sulfonic-acid model of colitis in humanized NOD/scid/gamma mice. Inhibition/blockade of antisense might represent a therapeutic strategy to restore CD39 along with immunohomeostasis in Crohn's disease.

Indexed as

AnimalsAntigens, CDApyraseCrohn DiseaseFemaleHumansMiceMice, Inbred NODRNA, AntisenseTh17 CellsT-Lymphocytes, RegulatoryAntigens, CDApyraseCD39 antigenRNA, Antisense

Identifiers

PMID33208731
PMCPMC7676266
OpenAlexW3105122483

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.