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dc.contributor.author | McGinley, Aoife M | |
dc.contributor.author | Sutton, Caroline E | |
dc.contributor.author | Edwards, Sarah C | |
dc.contributor.author | Leane, Charlotte M | |
dc.contributor.author | DeCourcey, Joseph | |
dc.contributor.author | Teijeiro, Ana | |
dc.contributor.author | Hamilton, John A | |
dc.contributor.author | Boon, Louis | |
dc.contributor.author | Djouder, Nabil | |
dc.contributor.author | Mills, Kingston H G | |
dc.date.accessioned | 2024-02-08T14:19:37Z | |
dc.date.available | 2024-02-08T14:19:37Z | |
dc.date.issued | 2020-02-18 | |
dc.identifier.citation | Immunity . 2020;52(2):342-356 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/17561 | |
dc.description.abstract | Interleukin-17A (IL-17A) is a major mediator of tissue inflammation in many autoimmune diseases. Anti-IL-17A is an effective treatment for psoriasis and is showing promise in clinical trials in multiple sclerosis. In this study, we find that IL-17A-defective mice or mice treated with anti-IL-17A at induction of experimental autoimmune encephalomyelitis (EAE) are resistant to disease and have defective priming of IL-17-secreting γδ T (γδT17) cells and Th17 cells. However, T cells from Il17a-/- mice induce EAE in wild-type mice following in vitro culture with autoantigen, IL-1β, and IL-23. Furthermore, treatment with IL-1β or IL-17A at induction of EAE restores disease in Il17a-/- mice. Importantly, mobilization of IL-1β-producing neutrophils and inflammatory monocytes and activation of γδT17 cells is reduced in Il17a-/- mice. Our findings demonstrate that a key function of IL-17A in central nervous system (CNS) autoimmunity is to recruit IL-1β-secreting myeloid cells that prime pathogenic γδT17 and Th17 cells. | es_ES |
dc.description.sponsorship | This work was supported by grants from Science Foundation Ireland (11/PI/1036, 16/IA/4468, and 12/RI/2340). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Cell Press | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Autoantigens | es_ES |
dc.subject.mesh | Autoimmunity | es_ES |
dc.subject.mesh | Central Nervous System | es_ES |
dc.subject.mesh | Encephalomyelitis, Autoimmune, Experimental | es_ES |
dc.subject.mesh | Interleukin-17 | es_ES |
dc.subject.mesh | Interleukin-1beta | es_ES |
dc.subject.mesh | Interleukin-23 | es_ES |
dc.subject.mesh | Intraepithelial Lymphocytes | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Mice, Inbred C57BL | es_ES |
dc.subject.mesh | Mice, Knockout | es_ES |
dc.subject.mesh | Monocytes | es_ES |
dc.subject.mesh | Myeloid Cells | es_ES |
dc.subject.mesh | Neutrophils | es_ES |
dc.subject.mesh | Th17 Cells | es_ES |
dc.title | Interleukin-17A Serves a Priming Role in Autoimmunity by Recruiting IL-1β-Producing Myeloid Cells that Promote Pathogenic T Cells. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 32023490 | es_ES |
dc.format.volume | 52 | es_ES |
dc.format.number | 2 | es_ES |
dc.format.page | 342 | es_ES |
dc.identifier.doi | 10.1016/j.immuni.2020.01.002 | es_ES |
dc.contributor.funder | Science Foundation Ireland | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1097-4180 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1016/j.immuni.2020.01.002. | es_ES |
dc.identifier.journal | Immunity | es_ES |
dc.repisalud.institucion | CNIO | es_ES |
dc.repisalud.orgCNIO | CNIO::Grupos de investigación::Grupo de Factores de Crecimiento, Nutrientes y Cáncer | es_ES |
dc.rights.accessRights | open access | es_ES |