ArticleMediators of inflammation2015
Deficits in endogenous adenosine formation by ecto-5'-nucleotidase/CD73 impair neuromuscular transmission and immune competence in experimental autoimmune myasthenia gravis.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- CD73: Friend or Foe in Lung Injury.International journal of molecular sciences · 2023Review
- Pharmacological Tuning of Adenosine Signal Nuances Underlying Heart Failure With Preserved Ejection Fraction.Frontiers in pharmacology · 2021Review
- Modulatory Roles of ATP and Adenosine in Cholinergic Neuromuscular Transmission.International journal of molecular sciences · 2020Review
- Article
- Ectonucleotidases in Acute and Chronic Inflammation.Frontiers in pharmacology · 2020Review
- Role of Cardiac AFrontiers in pharmacology · 2020Review
- The Purinergic System as a Pharmacological Target for the Treatment of Immune-Mediated Inflammatory Diseases.Pharmacological reviews · 2019Review
- Metabolic control of T cell immune response through glycans in inflammatory bowel disease.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Synaptic Homeostasis and Its Immunological Disturbance in Neuromuscular Junction Disorders.International journal of molecular sciences · 2017Review
- Purines and Carotid Body: New Roles in Pathological Conditions.Frontiers in pharmacology · 2017Review
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
- The role of adenosinergic pathway in human autoimmune diseases.Immunologic research · 2016Review
- Repeated Electroacupuncture Persistently Elevates Adenosine and Ameliorates Collagen-Induced Arthritis in Rats.Evidence-based complementary and alternative medicine : eCAM · 2016Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AMP dephosphorylation via ecto-5'-nucleotidase/CD73 is the rate limiting step to generate extracellular adenosine (ADO) from released adenine nucleotides. ADO, via A2A receptors (A2ARs), is a potent modulator of neuromuscular and immunological responses. The pivotal role of ecto-5'-nucleotidase/CD73, in controlling extracellular ADO formation, prompted us to investigate its role in a rat model of experimental autoimmune myasthenia gravis (EAMG). Results show that CD4(+)CD25(+)FoxP3(+) regulatory T cells express lower amounts of ecto-5'-nucleotidase/CD73 as compared to controls. Reduction of endogenous ADO formation might explain why proliferation of CD4(+) T cells failed upon blocking A2A receptors activation with ZM241385 or adenosine deaminase in EAMG animals. Deficits in ADO also contribute to neuromuscular transmission failure in EAMG rats. Rehabilitation of A2AR-mediated immune suppression and facilitation of transmitter release were observed by incubating the cells with the nucleoside precursor, AMP. These findings, together with the characteristic increase in serum adenosine deaminase activity of MG patients, strengthen our hypothesis that the adenosinergic pathway may be dysfunctional in EAMG. Given that endogenous ADO formation is balanced by ecto-5'-nucleotidase/CD73 activity and that A2ARs exert a dual role to restore use-dependent neurocompetence and immune suppression in myasthenics, we hypothesize that stimulation of the two mechanisms may have therapeutic potential in MG.
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