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dc.contributor.authorPuñet-Ortiz, Joan
dc.contributor.authorSáez Moya, Manuel
dc.contributor.authorCuenca, Marta
dc.contributor.authorCaleiras, E 
dc.contributor.authorLazaro, Adriana
dc.contributor.authorEngel, Pablo
dc.date.accessioned2019-09-17T06:17:44Z
dc.date.available2019-09-17T06:17:44Z
dc.date.issued2018-11-16
dc.identifier.citationFront Immunol. 2018;9:2661.es_ES
dc.identifier.issn1664-3224es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8354
dc.description.abstractSjögren's Syndrome (SjS) is a common chronic autoimmune disease characterized by the B cell hyperactivation, lymphocyte infiltration, and tissue damage of exocrine glands. It can also present life-threatening extraglandular manifestations, such as pulmonary and hepatic involvement, renal inflammation and marginal zone (MZ) B cell lymphoma. Several biologic agents have been tested in SjS but none has shown significant efficacy. Here, we report the effects of Ly9 (CD229) antibody targeting, a cell surface molecule that belongs to the SLAM family of immunomodulatory receptors, using NOD.H-2h4 mice as a model of SjS-like disease. Female mice were treated with anti-Ly9 antibody or isotype control at week 24, when all mice present SjS related autoantibodies, salivary gland infiltrates, and marginal zone (MZ) B cell pool enlargement. Antibody injection depleted key lymphocyte subsets involved in SjS pathology such as MZ, B1, and germinal center B cells in spleen and draining lymph nodes without inducing a general immunosuppression. Importantly, mice receiving anti-Ly9 mAb showed a reduced lymphocyte infiltrate within salivary glands. This reduction may be, in part, explained by the down-regulation of L-selectin and alfa4/beta7 integrin induced by the anti-Ly9 antibody. Furthermore, levels of anti-nuclear autoantibodies were reduced after anti-Ly9 treatment. These data indicate that Ly9 is a potential therapeutic target for the treatment of SjS.es_ES
dc.description.sponsorshipThe authors thank the NIH tetramer Core Facility for provision of PBS-57-loaded mCD1d tetramers. This work was supported by the Ministerio de Economia y Competividad through Grant SAF2015-69829-R (to PE).es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Media es_ES
dc.type.hasVersionVoRes_ES
dc.subjectLy9es_ES
dc.subjectSLAM family receptorses_ES
dc.subjectSjögren's Syndromees_ES
dc.subjectAntibody targetinges_ES
dc.subjectAutoimmunityes_ES
dc.titleLy9 (CD229) Antibody Targeting Depletes Marginal Zone and Germinal Center B Cells in Lymphoid Tissues and Reduces Salivary Gland Inflammation in a Mouse Model of Sjögren's Syndromees_ES
dc.typejournal articlees_ES
dc.identifier.pubmedID30519241es_ES
dc.format.volume9es_ES
dc.format.page2661es_ES
dc.identifier.doi10.3389/fimmu.2018.02661es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1664-3224es_ES
dc.relation.publisherversionhttps://doi.org/ 10.3389/fimmu.2018.02661.es_ES
dc.identifier.journalFrontiers in immunologyes_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Unidades técnicas::Unidad de Histopatologíaes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2015-69829-Res_ES
dc.rights.accessRightsopen accesses_ES


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