CD73 and CD39 ectonucleotidases in T cell differentiation: Beyond immunosuppression
Author
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Bono Merino, María Rosa
Author
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Fernández, Dominique
Author
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Flores Santibáñez, Felipe
Author
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Rosemblatt Silber, Mario César
Author
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Sauma Mahaluf, Daniela
Admission date
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2015-12-29T03:39:08Z
Available date
dc.date.available
2015-12-29T03:39:08Z
Publication date
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2015
Cita de ítem
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FEBS Letters 589 (2015) 3454–3460
en_US
Identifier
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DOI: 10.1016/j.febslet.2015.07.027
Identifier
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https://repositorio.uchile.cl/handle/2250/136015
General note
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Artículo de publicación ISI
en_US
Abstract
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Extracellular ATP is a danger signal released by dying and damaged cells, and it functions as an immunostimulatory signal that promotes inflammation. However, extracellular adenosine acts as an immunoregulatory signal that modulates the function of several cellular components of the adaptive and innate immune response. Consequently, the balance between ATP and adenosine concentration is crucial in immune homeostasis. CD39 and CD73 are two ectonucleoddases that cooperate in the generation of extracellular adenosine through ATP hydrolysis, thus tilting the balance towards immunosuppressive microenvironments. Extracellular adenosine can prevent activation, proliferation, cytokine production and cytotoxicity in T cells through the stimulation of the A2A receptor; however, recent evidence has shown that adenosine may also affect other processes in T-cell biology. In this review, we discuss evidence that supports a role of CD73 and CD39 ectonucleotidases in controlling naive T-cell homeostasis and memory cell survival through adenosine production. Finally, we propose a novel hypothesis of a possible role of these ectonucleotidases and autocrine adenosine signaling in controlling T-cell differentiation.