ArticleJournal of Crohn's & colitis2020
Modulation of CD39 and Exogenous APT102 Correct Immune Dysfunction in Experimental Colitis and Crohn's Disease.
Article in Journal of Crohn's & colitis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Dysregulation of CD39/Ectonucleoside Triphosphate Diphosphohydrolase 1 Causes Urinary Bladder Dysfunction with Abnormal Smooth Muscle Contractility.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Impact of Estrogen on Purinergic Signaling in Microvascular Disease.International journal of molecular sciences · 2025Review
- Article
- Blockade of PGK1 and ALDOA enhances bilirubin control of Th17 cells in Crohn's disease.Communications biology · 2022Article
- Biologic Agents in Crohn's Patients Reduce CD4Canadian journal of gastroenterology & hepatology · 2022Article
- Treatment-refractory ulcerative colitis responsive to indigo naturalis.BMJ open gastroenterology · 2021Article
- Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis.International journal of molecular sciences · 2021Review
- Synapomorphic features of hepatic and pulmonary vasculatures include comparable purinergic signaling responses in host defense and modulation of inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Targeting ectonucleotidases to treat inflammation and halt cancer development in the gut.Biochemical pharmacology · 2021Review
- Altered aryl-hydrocarbon-receptor signalling affects regulatory and effector cell immunity in autoimmune hepatitis.Journal of hepatology · 2021Article
- Dysfunctional Immune Regulation in Autoimmune Hepatitis: From Pathogenesis to Novel Therapies.Frontiers in immunology · 2021Review
- P2X7R: pivotal player in sepsis-induced liver damage.Purinergic signalling · 2020Article
- Endogenous antisense RNA curbs CD39 expression in Crohn's disease.Nature communications · 2020Article
- Ectonucleotidase Modulation of Lymphocyte Function in Gut and Liver.Frontiers in cell and developmental biology · 2020Review
- Purinergic Signaling in Controlling Macrophage and T Cell Functions During Atherosclerosis Development.Frontiers in immunology · 2020Review
- Control of Gut Inflammation by Modulation of Purinergic Signaling.Frontiers in immunology · 2020Review
- Eosinophils and Purinergic Signaling in Health and Disease.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsCD39/ENTPD1 scavenges pro-inflammatory nucleotides, to ultimately generate immunosuppressive adenosine, which has a central role in immune homeostasis. Global deletion of Cd39 increases susceptibility to experimental colitis while single nucleotide polymorphisms within the human CD39 promoter, and aberrant patterns of expression during experimental hypoxia, predispose to Crohn's disease. We aimed to define the impact of transgenic human CD39 [hTG] overexpression in experimental colitis and to model therapeutic effects using the recombinant apyrase APT102 in vivo. We also determined the in vitro effects of APT102 on phenotypic and functional properties of regulatory T-lymphocytes derived from patients with Crohn's disease.
methodsColitis was induced by administration of dextran sulfate sodium in wild-type [WT] or hTG mice, and, in another model, by adoptive transfer of CD45RBhigh cells with or without WT or hTG regulatory T cells [Treg]. In additional experiments, mice were treated with APT102. The effects of APT102 on phenotype and function of Treg and type-1 regulatory T [Tr1] cells were also evaluated, after purification from peripheral blood and lamina propria of Crohn's disease patients [n = 38].
resultsOverexpression of human CD39 attenuated experimental colitis and protected from the deleterious effects of systemic hypoxia, pharmacologically induced by deferoxamine. Administration of APT102 in vivo enhanced the beneficial effects of endogenous Cd39 boosted by the administration of the aryl hydrocarbon receptor [AhR] ligand unconjugated bilirubin [UCB]. Importantly, supplemental APT102 restored responsiveness to AhR stimulation by UCB in Treg and Tr1 cells, obtained from Crohn's disease patients.
conclusionshCD39 overexpression ameliorated experimental colitis and prevented hypoxia-related damage in vivo. Exogenous administration of APT102 boosted AhR-mediated regulatory effects in vivo while enhancing Treg functions in Crohn's disease in vitro.
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