dc.contributor.author | YANEZ MENESES, LUZ FRANCY | |
dc.contributor.author | Gajardo Carrasco, Tania Fernanda | |
dc.contributor.author | Pérez Béssolo, Francisco Andrés | |
dc.contributor.author | Terraza-Aguirre, Claudia | |
dc.contributor.author | Campos-Mora, Mauricio | |
dc.contributor.author | Pino Lagos, Karina | |
dc.date.accessioned | 2022-03-27T01:10:47Z | |
dc.date.available | 2022-03-27T01:10:47Z | |
dc.date.issued | 2015-06-02 | |
dc.identifier.uri | https://repositorio.ufps.edu.co/handle/ufps/6433 | |
dc.description.abstract | 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 regulator of immune tolerance by affecting regulatory T cells (Tregs); although the mechanism is not fully understood, it seems that dendritic cells and myeloid suppressor-derived cells may be cooperating in the generation and/or establishment of IL-33-mediated tolerance. Here, we review the most updated literature on IL-33, its role on T cell biology, and its impact in immune tolerance. | eng |
dc.format.extent | 8 Páginas | spa |
dc.format.mimetype | application/pdf | spa |
dc.language.iso | eng | spa |
dc.publisher | Frontiers in Immunology | spa |
dc.relation.ispartof | Frontiers in Immunology ISSN: 1664-3224, 2015 vol:6 fasc: N/A págs: - , DOI:10.3389/fimmu.2015.00232 | |
dc.rights | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). | eng |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | spa |
dc.source | https://www.frontiersin.org/articles/10.3389/fimmu.2015.00232/full | spa |
dc.title | Alarmin’ immunologists: IL-33 as a putative target for modulating T cell-dependent responses | eng |
dc.type | Artículo de revista | spa |
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dc.identifier.doi | https://doi.org/10.3389/fimmu.2015.00232 | |
dc.publisher.place | Chile | spa |
dc.relation.citationedition | Vol. 6 No. (2015) | spa |
dc.relation.citationendpage | 8 | spa |
dc.relation.citationissue | (2015) | spa |
dc.relation.citationstartpage | 1 | spa |
dc.relation.citationvolume | 6 | spa |
dc.relation.cites | Gajardo Carrasco T, Morales RA, Pérez F, Terraza C, Yáñez L, Campos-Mora M and Pino-Lagos K (2015) Alarmin’ immunologists: IL-33 as a putative target for modulating T cell-dependent responses. Front. Immunol. 6:232. doi: 10.3389/fimmu.2015.00232 | |
dc.relation.ispartofjournal | Frontiers in Immunology | spa |
dc.rights.accessrights | info:eu-repo/semantics/openAccess | spa |
dc.rights.creativecommons | Atribución 4.0 Internacional (CC BY 4.0) | spa |
dc.subject.proposal | iL-33 | eng |
dc.subject.proposal | T cells | eng |
dc.subject.proposal | tolerance | eng |
dc.subject.proposal | Transplantation | eng |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | spa |
dc.type.content | Text | spa |
dc.type.driver | info:eu-repo/semantics/article | spa |
dc.type.redcol | http://purl.org/redcol/resource_type/ARTREV | spa |
oaire.accessrights | http://purl.org/coar/access_right/c_abf2 | spa |
oaire.version | http://purl.org/coar/version/c_970fb48d4fbd8a85 | spa |
dc.type.version | info:eu-repo/semantics/publishedVersion | spa |