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Authordc.contributor.authorCarrasco, Tania Gajardo 
Authordc.contributor.authorMorales, Rodrigo A. 
Authordc.contributor.authorPérez, Francisco 
Authordc.contributor.authorTerraza, Claudia 
Authordc.contributor.authorYáñez, Luz 
Authordc.contributor.authorCampos Mora, Mauricio 
Authordc.contributor.authorPino Lagos, Karina 
Admission datedc.date.accessioned2019-03-18T11:53:04Z
Available datedc.date.available2019-03-18T11:53:04Z
Publication datedc.date.issued2015
Cita de ítemdc.identifier.citationFrontiers in Immunology, Volumen 6, Issue JUN, 2018,
Identifierdc.identifier.issn16643224
Identifierdc.identifier.other10.3389/fimmu.2015.00232
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/166588
Abstractdc.description.abstract© 2015 Gajardo Carrasco, Morales, Pérez, Terraza, Yáñez, Campos-Mora and Pino-Lagos. IL-33 is a known member of the IL-1 cytokine superfamily classically named "atypical" due to its diverse functions. The receptor for this cytokine is the ST2 chain (or IL-1RL1), part of the IL-1R family, and the accessory chain IL-1R. ST2 can be found as both soluble and membrane-bound forms, property that explains, at least in part, its wide range of functions. IL-33 has increasingly gained our attention as a potential target to modulate immune responses. At the beginning, it was known as one of the participants during the development of allergic states and other Th2-mediated responses and it is now accepted that IL-33 contributes to Th1-driven pathologies as demonstrated in animal models of experimental autoimmune encephalomyelitis (EAE), collagen-induced arthritis, and trinitrobenzene sulfonic acid-induced experimental colitis, among others. Interestingly, current data are placing IL-33 as a novel r
Lenguagedc.language.isoen
Publisherdc.publisherFrontiers Media S.A.
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Sourcedc.sourceFrontiers in Immunology
Keywordsdc.subjectIl-33
Keywordsdc.subjectT cells
Keywordsdc.subjectTolerance
Keywordsdc.subjectTransplantation
Títulodc.titleAlarmin' immunologists: IL-33 as a putative target for modulating T cell-dependent responses
Document typedc.typeArtículo de revista
dcterms.accessRightsdcterms.accessRightsAcceso Abierto
Catalogueruchile.catalogadorSCOPUS
Indexationuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile