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dc.contributor.advisorShoenfeld, Yehuda 
dc.contributor.advisorBlank, Miri 
dc.creatorArango, María-Teresa 
dc.date.accessioned2017-02-06T15:22:20Z
dc.date.available2017-02-06T15:22:20Z
dc.date.created2016-10-24
dc.date.issued2016
dc.identifier.urihttp://repository.urosario.edu.co/handle/10336/12875
dc.descriptionLas anormalidades de comportamiento y disfunciones cognitivas pueden presentarse en pacientes con enfermedades autoinmunes. Estos síntomas pueden fluctuar de leves hasta eventos potencialmente mortales. En su gran mayoría los mecanismos responsables de estas manifestaciones neuropsiquiatricas siguen siendo desconocidas, sin embargo se han identificado varias vías patogénicas. Por ejemplo; neurotoxicidad mediada por anticuerpos, vasculopatía inducida por anticuerpos anti-fosfolípidos, neurotoxicidad inducida por citoquinas, así como factores externos que incluyen sustancias tóxicas y medicamentos. Para poder investigar algunos de estos mecanismos, evaluamos el efecto de auto-anticuerpos relacionados con el lupus eritematoso sistémico neuropsiquiátrico en modelos animales (Anticuerpo idiotípico 16/6 y el anticuerpo anti-ribosoma P) y narcolepsia (empleando IgG de pacientes narcolépticos), así como el efecto de la vacuna del virus del papiloma humano en ratones. La inmunización pasiva por inyección intracerebro-ventricular de estos anticuerpos condujo a cambios histológicos, cognitivos y de comportamiento. En particular, los ratones inmunizados con el anticuerpo idiotípico 16/6 desarrollaron déficit cognitivo y los ratones inmunizados con el anticuerpo anti-ribosomal P desarrollaron depresión. Los ratones que recibieron IgG total de pacientes narcolépticos desarrollaron trastornos del sueño y cambios histológicos cerebrales consistentes con la enfermedad. Un análisis más profundo del papel del anticuerpo anti-ribosomal P humano reveló que reacciona de manera cruzada con la proteína neuronal “Gap43” interfiriendo con procesos celulares. Por otra parte, la inmunización con la vacuna del virus del papiloma humano causó la producción de anticuerpos contra componentes del cerebro. Adicionalmente, los ratones inmunizados con la vacuna, al igual que los inmunizados con su adyuvante desarrollaron deficiencia cognitiva y conductual, que fue mejorada con la suplementación alimenticia basada en fosfolípidos. En general, aquí se demuestra que anormalidades del comportamiento y disfunciones cognitiva pueden ser parte de la amplia gama de manifestaciones clínicas autoinmunes. Además, nuestros resultados sugieren que estas pueden ser causadas por daños colaterales debido a la desregulación inmune causada por autoinmunidad, así como por la vacunación. Adicionalmente, sugerimos que diferentes auto-anticuerpos causan diferentes síntomas basados en diferentes interacciones con el tejido cerebral.
dc.description.abstractBehavioral abnormalities and cognitive dysfunction may be present in patients with autoimmune diseases. The mechanisms that responsible for these neuropsychiatric manifestations are still largely unknown, however several pathogenic pathways have been identified such as antibody damage, cytokine-induced neurotoxicity, as well as external factors like toxics, and medications. To further investigate some of these mechanisms we evaluated the effect of autoantibodies in animal models of neuropsychiatric systemic lupus erythematosus and narcolepsy, and the effect of the human papillomavirus vaccine in naïve mice. Using the passive immunization method through intracerebro-ventricular injection of the antibodies, we demonstrated histological and behavioral changes. Mice immunized with 16/6 idiotypic antibodies developed cognitive impairments while those immunized with anti-ribosomal-P antibodies developed depression. The mice that received total IgG from narcoleptic patients developed sleep disturbances and brain histological changes. Further analyses of the role of the human anti-ribosomal-P autoantibody revealed that it can cross-react with the neuronal protein Gap43, interfering with cellular processes. Immunization with the human papillomavirus vaccine induced the production of brain antibodies. Moreover, the mice immunized with the vaccine or with its adjuvant developed cognitive and behavioral deficiencies, which were ameliorated with dietary phospholipid supplementation. Overall, herein we demonstrate that the behavioral and cognitive abnormalities can be part of the wide spectrum of clinical autoimmune manifestations. In addition, they can be caused by collateral damage due to the immune dysregulation caused by autoimmune conditions as well as by vaccination. We also suggest that different autoantibodies cause different symptoms based on different interactions with brain tissue.
dc.description.sponsorshipColton Foundation
dc.description.sponsorshipFederico Foundation
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.5/co/
dc.sourceinstname:Universidad del Rosario
dc.sourcereponame:Repositorio Institucional EdocUR
dc.subjectTejido Cerebral
dc.subjectLupus eritematoso sistémico
dc.subjectNarcolepsia
dc.subjectAutoanticuerpos
dc.subjectVacunas
dc.subjectVPH
dc.subject.ddcFisiología humana 
dc.subject.lembCerebro
dc.titleAutoantibody and environmental damage to the brain
dc.typedoctoralThesis
dc.publisherUniversidad del Rosario
dc.creator.degreeDoctor en Ciencias Biomédicas
dc.publisher.programDoctorado en Ciencias Biomédicas
dc.publisher.departmentFacultad de Ciencias Naturales y Matemáticas
dc.subject.keywordBrain
dc.subject.keywordAutoantibodies
dc.subject.keywordSLE
dc.subject.keywordNarcolepsy
dc.subject.keywordVaccines
dc.subject.keywordHPV
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.subject.decsLupus Eritematoso Sistémico
dc.subject.decsNarcolepsia
dc.subject.decsAutoanticuerpos
dc.subject.decsPapillomavirus Humano
dc.subject.decsTesis y disertaciones académicas
dc.type.spaTesis de doctorado
dc.rights.accesoAbierto (Texto completo)
dc.type.hasVersioninfo:eu-repo/semantics/acceptedVersion
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dc.title.TranslatedTitleEfecto de autoanticuerpos y factores ambientales en el cerebro


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