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GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection

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dc.contributor.author Ortiz Wilczyñski, Juan M.
dc.contributor.author Olexen, Cinthia M.
dc.contributor.author Errasti, Andrea E.
dc.contributor.author Schattner, Mirta
dc.contributor.author Rothlin, Carla V.
dc.contributor.author Correale, Jorge
dc.contributor.author Carrera Silva, Eugenio A.
dc.date.accessioned 2021-04-30T12:39:15Z
dc.date.available 2021-04-30T12:39:15Z
dc.date.issued 2020-11-21
dc.identifier.citation Ortiz Wilczyñski JM, Olexen CM, Errasti AE, Schattner M, Rothlin CV, Correale J, Carrera Silva EA. GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection. PLoS Pathog. 2020 Dec 21;16(12):e1009176. doi: 10.1371/journal.ppat.1009176. PMID: 33347509 es_ES
dc.identifier.uri https://repositorio.fleni.org.ar/xmlui/handle/123456789/446
dc.identifier.uri https://doi.org/10.1371/journal.ppat.1009176
dc.description.abstract Multiple sclerosis (MS) is a highly disabling neurodegenerative autoimmune condition in which an unbalanced immune response plays a critical role. Although the mechanisms remain poorly defined, helminth infections are known to modulate the severity and progression of chronic inflammatory diseases. The tyrosine kinase receptors TYRO3, AXL, and MERTK (TAM) have been described as inhibitors of the immune response in various inflammatory settings. We show here that patients with concurrent natural helminth infections and MS condition (HIMS) had an increased expression of the negative regulatory TAM receptors in antigen-presenting cells and their agonist GAS6 in circulating CD11bhigh and CD4+ T cells compared to patients with only MS. The Th17 subset was reduced in patients with HIMS with a subsequent downregulation of its pathogenic genetic program. Moreover, these CD4+ T cells promoted lower levels of the co-stimulatory molecules CD80, CD86, and CD40 on dendritic cells compared with CD4+ T cells from patients with MS, an effect that was GAS6-dependent. IL-10+ cells from patients with HIMS showed higher GAS6 expression levels than Th17 cells, and inhibition of phosphatidylserine/GAS6 binding led to an expansion of Th17 effector genes. The addition of GAS6 on activated CD4+ T cells from patients with MS restrains the Th17 gene expression signature. This cohort of patients with HIMS unravels a promising regulatory mechanism to dampen the Th17 inflammatory response in autoimmunity. es_ES
dc.language.iso eng es_ES
dc.publisher Public Library of Science es_ES
dc.rights info:eu-repo/semantics/openAccess
dc.rights.uri https://creativecommons.org/licenses/by/2.5/ar/
dc.subject Multiple Sclerosis es_ES
dc.subject Esclerosis Múltiple es_ES
dc.subject Th17 Cells es_ES
dc.subject Células Th17 es_ES
dc.title GAS6 signaling tempers Th17 development in patients with multiple sclerosis and helminth infection es_ES
dc.type info:eu-repo/semantics/article es_ES
dc.type info:eu-repo/semantics/publishedVersion
dc.description.fil Fil: Correale, Jorge. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.
dc.description.fil Fil: Ortiz Wilczyñski, Juan M. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental; Argentina.
dc.description.fil Fil: Olexen, Cinthia M. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental; Argentina.
dc.description.fil Fil: Errasti, Andrea E. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Farmacología; Argentina.
dc.description.fil Fil: Schattner, Mirta. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental; Argentina.
dc.description.fil Fil: Carrera Silva, Eugenio A. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental; Argentina.
dc.description.fil Fil: Rothlin, Carla V. Yale University. Department of Immunobiology and Pharmacology; Estados Unidos.
dc.relation.ispartofVOLUME 16
dc.relation.ispartofNUMBER 12
dc.relation.ispartofPAGINATION e1009176.
dc.relation.ispartofCOUNTRY Estados Unidos
dc.relation.ispartofCITY San Francisco
dc.relation.ispartofTITLE PLoS pathogens
dc.relation.ispartofISSN 1553-7374
dc.type.snrd info:ar-repo/semantics/artículo es_ES


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