Deficits in Endogenous Adenosine Formation by Ecto-5′-NucleotidaseCD73 Impair Neuromuscular Transmission and Immune Competence in Experimental Autoimmune Myasthenia Gravis
المؤلفون المشاركون
Magalhães-Cardoso, Maria Teresa
Ferreirinha, Fátima
Correia-de-Sá, Paulo
Oliveira, Laura
Correia, Alexandra
Cristina Costa, Ana
Guerra-Gomes, Sónia
Vilanova, Manuel
المصدر
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-16، 16ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-01-27
دولة النشر
مصر
عدد الصفحات
16
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1072367
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر