Purinergic Signaling as a Regulator of Th17 Cell Plasticity

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dc.contributor.authorFernández, Dominique
dc.contributor.authorFlores-Santibáñez, Felipe
dc.contributor.authorNeira, Jocelyn
dc.contributor.authorOsorio-Barrios, Francisco
dc.contributor.authorTejón, Gabriela
dc.contributor.authorNuñez, Sarah
dc.contributor.authorHidalgo, Yessia
dc.contributor.authorFuenzalida, Maria Jose
dc.contributor.authorMeza, Daniel
dc.contributor.authorUreta, Gonzalo
dc.contributor.authorLladser, Alvaro
dc.contributor.authorPacheco, Rodrigo
dc.contributor.authorAcuña-Castillo, Claudio
dc.contributor.authorGuixé, Victoria
dc.contributor.authorQuintana, Francisco J.
dc.contributor.authorBono, Maria Rosa
dc.contributor.authorRosemblatt, Mario
dc.contributor.authorSauma, Daniela
dc.date.accessioned2016-07-22T15:22:42Z
dc.date.available2016-07-22T15:22:42Z
dc.date.issued2016-06
dc.descriptionIndexación: Web of Sciencees
dc.description.abstractT helper type 17 (Th17) lymphocytes, characterized by the production of interleukin-17 and other pro-inflammatory cytokines, are present in intestinal lamina propria and have been described as important players driving intestinal inflammation. Recent evidence, supporting the notion of a functional and phenotypic instability of Th17 cells, has shown that Th17 differentiate into type 1 regulatory (Tr1) T cells during the resolution of intestinal inflammation. Moreover, it has been suggested that the expression of CD39 ectonucleotidase endows Th17 cells with immunosuppressive properties. However, the exact role of CD39 ectonucleotidase in Th17 cells has not been studied in the context of intestinal inflammation. Here we show that Th17 cells expressing CD39 ectonucleotidase can hydrolyze ATP and survive to ATP-induced cell death. Moreover, in vitro-generated Th17 cells expressing the CD39 ectonucleotidase produce IL-10 and are less pathogenic than CD39 negative Th17 cells in a model of experimental colitis in Rag-/- mice. Remarkably, we show that CD39 activity regulates the conversion of Th17 cells to IL-10-producing cells in vitro, which is abrogated in the presence of ATP and the CD39-specific inhibitor ARL67156. All these data suggest that CD39 expression by Th17 cells allows the depletion of ATP and is crucial for IL-10 production and survival during the resolution of intestinal inflammation.es
dc.description.urihttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0157889
dc.identifier.citationPLoS ONE 11(6): e0157889es
dc.identifier.issn1932-6203
dc.identifier.otherhttp://dx.doi.org/10.1371/journal.pone.0157889
dc.identifier.urihttp://repositorio.unab.cl/xmlui/handle/ria/1138
dc.language.isoenes
dc.publisherPUBLIC LIBRARY SCIENCEes
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectINFLAMMATORY-BOWEL-DISEASEes
dc.subjectPATHOGENIC T(H)17 CELLSes
dc.subjectCYTOKINE GM-CSFes
dc.subjectT-CELLSes
dc.subjectCROHNS-DISEASEes
dc.subjectADENOSINE GENERATIONes
dc.subjectIMMUNE SUPPRESSIONes
dc.subjectADAPTIVE IMMUNITYes
dc.subjectTYPE-1 CELLSes
dc.subjectTGF-BETAes
dc.titlePurinergic Signaling as a Regulator of Th17 Cell Plasticityes
dc.typeArtículoes
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