Evidence map›Paper›PMID 25661084›Full record

ArticleTransplant immunology2015

CD39 deficiency in murine liver allografts promotes inflammatory injury and immune-mediated rejection.

Osamu Yoshida, Lei Dou, Shoko Kimura, Shinichiro Yokota, Kumiko Isse, Simon C Robson, David A Geller, Angus W Thomson

Open access · greenAbstract read
In one paragraph

Article in Transplant immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Mouse orthotopic liver transplantation: Challenges, achievements, and applications.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Extracellular nucleotide signaling in solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Review
  8. Intrahepatic TFrontiers in pharmacology · 2020
    Review
  9. Macrophages in xenotransplantation.Korean journal of transplantation · 2019
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. [Effect of inhibiting TIM-4 function in Kupffer cells on liver graft rejection in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2016
    Article
  17. Liver transplantation in the mouse: Insights into liver immunobiology, tissue injury, and allograft tolerance.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2016
    Review
  18. 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

8 authors at 3 institutions in 1 country.

Osamu YoshidaStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: osamuyoishida@yahoo.co.jp.
Lei DouStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: doul@upmc.edu.
Shoko KimuraStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: kimuras@upmc.edu.
Shinichiro YokotaStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: yokotas@upmc.edu.
Kumiko IsseStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: issek@upmc.edu.
Simon C RobsonDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. Electronic address: srobson@bidmc.harvard.edu.
David A GellerStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; University of Pittsburgh Medical Center, Liver Cancer Center, Pittsburgh, PA, USA. Electronic address: gellerda@upmc.edu.
Angus W ThomsonStarzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: thomsonaw@upmc.edu.
University of Pittsburgh · USBeth Israel Deaconess Medical Center · USUniversity of Pittsburgh Medical Center · US

Funding

Interdisciplinary Training in Transplantation BiologyT32AI074490 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Angus W Thomson · 2007 to 2026
$4.2M
Liver Antigen - Presenting Cells in Hepatic Injury and TransplantationP01AI081678 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI THOMSON, ANGUS W · 2009 to 2010
$2.8M
NIAID NIH HHS NIH T32AI74490NIAID NIH HHS P01 AI081678NIAID NIH HHS P01AI81678NIAID NIH HHS T32 AI074490
6 · The paper itself

Abstract

Adenosine triphosphate (ATP), an essential metabolic energy source, is released following cell apoptosis or necrosis. It acts as a damage-associated molecule pattern to stimulate innate immune cells. The ectonucleotidase CD39 regulates immune activation by hydrolysis of extracellular ATP. We have shown previously that CD39 expression by donor livers helps protect syngeneic grafts with extended (24h) cold preservation time from ischemia reperfusion injury. Given its immune regulatory properties, we hypothesized that CD39 expression in donor livers might modulate transplant tolerance that occurs following mouse allogeneic liver transplantation (LTx). Livers from C57BL/6 (B6) wild-type (WT) or CD39 KO mice were transplanted into normal C3H recipients with minimal (approximately 1h) cold ischemia. Serum alanine aminotransferase levels at day 4 post-LTx were significantly higher in animals given CD39KO compared with WT livers. Moreover, IFN-γ production by liver-infiltrating CD8(+) T cells at day 4 was significantly higher in CD39KO than in WT grafts. Furthermore, splenic T cells from CD39KO liver recipients exhibited greater proliferative responses to donor alloantigens than those from mice given WT grafts. By contrast, there was a concomitant significant reduction in the frequency of regulatory T cells (Treg) in CD39KO than in WT livers. Whereas WT liver allografts survived >100 days, no CD39KO grafts survived beyond 40 days (median survival time [MST]: WT: >100 days vs CD39KO: 8 days; p<0.01). In addition, soluble CD39 administration significantly prolonged CD39KO liver allograft survival (MST: 27.5 days). These novel data suggest that CD39 expression in liver allografts modulates tissue injury, inflammation, anti-donor effector T cell responses and Treg infiltration and can suppress transplant rejection.

Indexed as

Graft RejectionHepatitisLiver TransplantationAllograftsAnimalsAntigens, CDApyraseGraft SurvivalMaleMiceMice, KnockoutAntigens, CDApyraseCD39 antigenAdenosine triphosphateCD39Liver allograftT cell

Identifiers

PMID25661084
PMCPMC4368493
OpenAlexW2035448361

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.