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Deficits in Endogenous Adenosine Formation by Ecto-5′-NucleotidaseCD73 Impair Neuromuscular Transmission and Immune Competence in Experimental Autoimmune Myasthenia Gravis
Joint Authors
Magalhães-Cardoso, Maria Teresa
Ferreirinha, Fátima
Correia-de-Sá, Paulo
Oliveira, Laura
Correia, Alexandra
Cristina Costa, Ana
Guerra-Gomes, Sónia
Vilanova, Manuel
Source
Issue
Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-16, 16 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-01-27
Country of Publication
Egypt
No. of Pages
16
Main Subjects
Abstract EN
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.
American Psychological Association (APA)
Oliveira, Laura& Correia, Alexandra& Cristina Costa, Ana& Guerra-Gomes, Sónia& Ferreirinha, Fátima& Magalhães-Cardoso, Maria Teresa…[et al.]. 2015. Deficits in Endogenous Adenosine Formation by Ecto-5′-NucleotidaseCD73 Impair Neuromuscular Transmission and Immune Competence in Experimental Autoimmune Myasthenia Gravis. Mediators of Inflammation،Vol. 2015, no. 2015, pp.1-16.
https://search.emarefa.net/detail/BIM-1072367
Modern Language Association (MLA)
Oliveira, Laura…[et al.]. Deficits in Endogenous Adenosine Formation by Ecto-5′-NucleotidaseCD73 Impair Neuromuscular Transmission and Immune Competence in Experimental Autoimmune Myasthenia Gravis. Mediators of Inflammation No. 2015 (2015), pp.1-16.
https://search.emarefa.net/detail/BIM-1072367
American Medical Association (AMA)
Oliveira, Laura& Correia, Alexandra& Cristina Costa, Ana& Guerra-Gomes, Sónia& Ferreirinha, Fátima& Magalhães-Cardoso, Maria Teresa…[et al.]. Deficits in Endogenous Adenosine Formation by Ecto-5′-NucleotidaseCD73 Impair Neuromuscular Transmission and Immune Competence in Experimental Autoimmune Myasthenia Gravis. Mediators of Inflammation. 2015. Vol. 2015, no. 2015, pp.1-16.
https://search.emarefa.net/detail/BIM-1072367
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1072367