dc.creatorZalosnik Figueroa, María Inés
dc.creatorFabio, Maria Carolina
dc.creatorBertoldi, María Laura
dc.creatorCastañares, Clara Nicole
dc.creatorDegano, Alicia Laura
dc.date.accessioned2022-08-17T15:23:10Z
dc.date.accessioned2022-10-15T13:18:43Z
dc.date.available2022-08-17T15:23:10Z
dc.date.available2022-10-15T13:18:43Z
dc.date.created2022-08-17T15:23:10Z
dc.date.issued2021-05
dc.identifierZalosnik Figueroa, María Inés; Fabio, Maria Carolina; Bertoldi, María Laura; Castañares, Clara Nicole; Degano, Alicia Laura; MeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge; Nature Research; Scientific Reports; 11; 1; 5-2021; 1-15
dc.identifierhttp://hdl.handle.net/11336/165840
dc.identifier2045-2322
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/4390573
dc.description.abstractRett syndrome is a severe and progressive neurological disorder linked to mutations in the MeCP2 gene. It has been suggested that immune alterations may play an active role in the generation and/or maintenance of RTT phenotypes. However, there is no clear consensus about which pathways are regulated in vivo by MeCP2 in the context of immune activation. In the present work we set to characterize the role of MeCP2 during the progression of Experimental Autoimmune Encephalomyelitis (EAE) using the MeCP2308/y mouse model (MUT), which represents a condition of “MeCP2 function deficiency”. Our results showed that MeCP2 deficiency increased the susceptibility to develop EAE, along with a defective induction of anti-inflammatory responses and an exacerbated MOG-specific IFNγ expression in immune sites. In MUT-EAE spinal cord, we found a chronic increase in pro-inflammatory cytokines gene expression (IFNγ, TNFα and IL-1β) and downregulation of genes involved in immune regulation (IL-10, FoxP3 and CX3CR1). Moreover, our results indicate that MeCP2 acts intrinsically upon immune activation, affecting neuroimmune homeostasis by regulating the pro-inflammatory/anti-inflammatory balance in vivo. These results are relevant to identify the potential consequences of MeCP2 mutations on immune homeostasis and to explore novel therapeutic strategies for MeCP2-related disorders.
dc.languageeng
dc.publisherNature Research
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://www.nature.com/articles/s41598-021-90517-8
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1038/s41598-021-90517-8
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectNeurodesarrollo
dc.subjectNeuroinmunologia
dc.subjectNeuroinflamacion
dc.titleMeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:ar-repo/semantics/artículo
dc.typeinfo:eu-repo/semantics/publishedVersion


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