ArticleBlood2012
Deficiency of CD73/ecto-5'-nucleotidase in mice enhances acute graft-versus-host disease.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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.
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.
Who cites it
48 citing papers in PubMed, 90 citations in OpenAlex.
- Trial
- Calcification of joints and arteries: second report with novel NT5E mutations and expansion of the phenotype.Journal of human genetics · 2015Trial
- Immune Escape of Acute Myeloid Leukemia after Transplantation.Blood cancer discovery · 2025Review
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Targeting CD73 and correcting adenosinergic signaling in critically ill patients.Frontiers in pharmacology · 2025Review
- A novel role of CD73-IFNγ signalling axis in human mesenchymal stromal cell mediated inflammatory macrophage suppression.Regenerative therapy · 2024Article
- Metabolic instruction of the graft-versus-leukemia immunity.Frontiers in immunology · 2024Review
- Relapse of acute myeloid leukemia after allogeneic stem cell transplantation: immune escape mechanisms and current implications for therapy.Molecular cancer · 2023Review
- Endothelial Effects of Simultaneous Expression of Human HO-1, E5NT, and ENTPD1 in a Mouse.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Purinergic receptor: a crucial regulator of adipose tissue functions.Purinergic signalling · 2023Review
- Editorial: Current concepts of cellular and biological drugs to modulate regulatory T cell activity in the clinic, volume II.Frontiers in immunology · 2023Article
- Immune function and dysfunction are determined by lymphoid tissue efficacy.Disease models & mechanisms · 2022Review
- Purinergic Signalling in Allogeneic Haematopoietic Stem Cell Transplantation and Graft-versus-Host Disease.International journal of molecular sciences · 2021Review
- CD73 Overexpression in Podocytes: A Novel Marker of Podocyte Injury in Human Kidney Disease.International journal of molecular sciences · 2021Article
- Targeting the purinergic pathway in breast cancer and its therapeutic applications.Purinergic signalling · 2021Review
- Use of Humanized Mouse Models to Investigate the Roles of Purinergic Signaling in Inflammation and Immunity.Frontiers in pharmacology · 2020Article
- Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies.Cancers · 2019Review
- Human ectoenzyme-expressing ILC3: immunosuppressive innate cells that are depleted in graft-versus-host disease.Blood advances · 2019Article
- An agonistic anti-Toll-like receptor 4 monoclonal antibody as an effective adjuvant for cancer immunotherapy.Immunology · 2019Article
- Achievement of Tolerance Induction to Prevent Acute Graft-vs.-Host Disease.Frontiers in immunology · 2019Review
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Extracellular ATP and adenosine have immunoregulatory roles during inflammation. Elevated extracellular ATP is known to exacerbate GVHD, and the pharmacologic activation of the adenosine A2A receptor is protective. However, the role of endogenous adenosine is unknown. We used gene-targeted mice and a pharmacologic inhibitor to test the role of adenosine generated by CD73/ecto-5'-nucleotidase in GVHD. In allogeneic transplants, both donor and recipient CD73 were protective, with recipient CD73 playing the dominant role. CD73 deficiency led to enhanced T-cell expansion and IFN-γ and IL-6 production, and the migratory capacity of Cd73-/- T cells in vitro was increased. However, the number of regulatory T cells and expression of costimulatory molecules on antigen-presenting cells were unchanged. A2A receptor deficiency led to increased numbers of allogeneic T cells, suggesting that signaling through the A2A receptor via CD73-generated adenosine is a significant part of the mechanism by which CD73 limits the severity of GVHD. Pharmacologic blockade of CD73 also enhanced graft-versus-tumor activity. These data have clinical implications, as both the severity of GVHD and the strength of an alloimmune antitumor response could be manipulated by enhancing or blocking CD73 activity or adenosine receptor signaling depending on the clinical indication.
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Registered trials
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.