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dc.contributor.authorBallester, Alicia 
dc.contributor.authorGuijarro, Adriana 
dc.contributor.authorBravo, Beatriz 
dc.contributor.authorHernandez, Javier R 
dc.contributor.authorMurillas, Rodolfo
dc.contributor.authorGallego, Marta Ines 
dc.contributor.authorBallester, Sara 
dc.date.accessioned2022-04-20T09:57:22Z
dc.date.available2022-04-20T09:57:22Z
dc.date.issued2022-03-15
dc.identifier.citationInt J Mol Sci. 2022;23(6):3171.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/14133
dc.description.abstractThe Hedgehog (Hh) pathway is essential for the embryonic development and homeostatic maintenance of many adult tissues and organs. It has also been associated with some functions of the innate and adaptive immune system. However, its involvement in the immune response has not been well determined. Here we study the role of Hh signalling in the modulation of the immune response by using the Ptch-1-LacZ+/- mouse model (hereinafter referred to as ptch+/-), in which the hemizygous inactivation of Patched-1, the Hh receptor gene, causes the constitutive activation of Hh response genes. The in vitro TCR stimulation of spleen and lymph node (LN) T cells showed increased levels of Th2 cytokines (IL-4 and IL-10) in ptch+/-cells compared to control cells from wild-type (wt) littermates, suggesting that the Th2 phenotype is favoured by Hh pathway activation. In addition, CD4+ cells secreted less IL-17, and the establishment of the Th1 phenotype was impaired in ptch+/- mice. Consistently, in response to an inflammatory challenge by the induction of experimental autoimmune encephalomyelitis (EAE), ptch+/- mice showed milder clinical scores and more minor spinal cord damage than wt mice. These results demonstrate a role for the Hh/ptch pathway in immune response modulation and highlight the usefulness of the ptch+/- mouse model for the study of T-cell-mediated diseases and for the search for new therapeutic strategies in inflammatory diseases.es_ES
dc.description.sponsorshipThe work was sponsored by grants from Acción Estratégica en Salud (PI17CIII/00047 and PI21/00171).es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectHedgehoges_ES
dc.subjectPatched-1es_ES
dc.subjectTh lymphocyteses_ES
dc.subjectExperimental autoimmune encephalomyelitises_ES
dc.subjectMultiple sclerosises_ES
dc.titleHedgehog Signalling Modulates Immune Response and Protects against Experimental Autoimmune Encephalomyelitis.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID35328591es_ES
dc.format.volume23es_ES
dc.format.number6es_ES
dc.format.page3171es_ES
dc.identifier.doi10.3390/ijms23063171es_ES
dc.contributor.funderInstituto de Salud Carlos III es_ES
dc.description.peerreviewedes_ES
dc.identifier.e-issn1422-0067es_ES
dc.relation.publisherversionhttps://doi.org/10.3390/ijms23063171es_ES
dc.identifier.journalInternational Journal of Molecular Scienceses_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/PI17CIII/00047es_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/PI21/00171es_ES


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