Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares

datacite.rightshttp://purl.org/coar/access_right/c_abf2
dc.contributor.authorVergara Serpa, Oscar Vicente
dc.contributor.authorApraez Mazabe, Nayla
dc.contributor.authorCórdoba Paredes, Juan Sebastián
dc.contributor.authorArenas Contreras, Erika Jhohanna
dc.contributor.authorLemus Arellano, Elva Rosa
dc.contributor.authorHerrera Olivares, Miguel Ángel
dc.contributor.authorRuiz Pastrana, Geraldine Lucia
dc.contributor.authorGrajales Marín, Vanesa Alejandra
dc.contributor.authorDaza Arnedo, Rodrigo
dc.contributor.authorVázquez Jiménez, Lourdes Carolina
dc.contributor.authorRico Fontalvo, Jorge
dc.date.accessioned2024-07-03T22:16:55Z
dc.date.available2024-07-03T22:16:55Z
dc.date.issued2024
dc.description.abstractIntroduction: El lupus eritematoso sistémico (LES) es una enfermedad autoinmune que causa inflamación sistémica y alteraciones en la tolerancia inmunológica. La activación de los genes inducibles por interferón (IFN), contribuye en más del 50 % de su patogenia. Objetivo: relacionar el papel del IFN-λ en la patogenia del LES. Materiales y Métodos: Búsqueda sistémica en base de datos; a través de las palabras claves del MeSH and DeCS. Fue incluido adicionalmente la palabra “Interferón Lambda”. Resultados: Se encontró que la producción aberrante de interferón tipo I contribuye a la desregulación de IFN-λ, producido principalmente por células dendríticas plasmocitoides. Este proceso conduce a la estimulación inmunológica por autoanticuerpos y a un aumento de IFNλR-1 en células B, potenciando la generación de anticuerpos. IFN-λ3 se asocia particularmente con nefritis lúpica, y el IFN-λ en general aumenta la expresión de MHC-I, intensificando la respuesta de células T CD8+ y posiblemente afectando la tolerancia central y la regulación en el timo. Conclusión: Se destaca que el IFN-λ favorece la activación inmune, formación de inmunocomplejos, inflamación crónica y producción de autoanticuerpos, vinculándose niveles altos de IFN-λ3 con mayor actividad de la enfermedad.spa
dc.description.abstractIntroduction: Systemic lupus erythematosus (SLE) is an autoimmune disease that causes systemic inflammation and alterations in immunological tolerance. The activation of interferon (IFN)-inducible genes contributes to more than 50% of its pathogenesis. Objective: to review the role of IFN-λ in the pathogenesis of SLE Materials and Methods: Systemic search in database; through the MeSH and DeCS keywords. The word “Lambda Interferon” was additionally included. Results: Aberrant production of type I interferon was found to contribute to the deregulation of IFN-λ, produced mainly by plasmacytoid dendritic cells. This process leads to immunological stimulation by autoantibodies and an increase in IFNλR-1 in B cells, enhancing the generation of antibodies. IFN-λ3 is particularly associated with lupus nephritis, and IFN-λ generally increases MHC-I expression, enhancing the CD8+ T cell response and possibly affecting central tolerance and regulation in the thymus. Conclusion: It is highlighted that IFN-λ favors immune activation, formation of immune complexes, chronic inflammation and production of autoantibodies, linking high levels of IFN-λ3 with greater disease activity.eng
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.18004/rpr/2024.10.01.37
dc.identifier.issn24134341 (En línea)
dc.identifier.urihttps://hdl.handle.net/20.500.12442/14801
dc.identifier.urlhttp://scielo.iics.una.py/scielo.php?script=sci_arttext&pid=S2413-43412024000100037&lng=es&nrm=iso&tlng=es
dc.language.isospa
dc.publisherSociedad Paraguaya de Reumatologíaspa
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United Stateseng
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/
dc.sourceRevista Paraguaya de Reumatologíaspa
dc.sourceRev. parag. reumatol.spa
dc.sourceVol. 10 No. 1, (2024)
dc.subjectAutoinmunidadspa
dc.subjectInterferonesspa
dc.subjectLupus eritematoso sistémicospa
dc.subjectReceptores Interferónspa
dc.subjectReceptores tipo Tollspa
dc.subject.keywordsAutoimmunityeng
dc.subject.keywordsInterferonseng
dc.subject.keywordsSystemic lupus erythematosuseng
dc.subject.keywordsInterferon receptorseng
dc.subject.keywordsToll-like receptorseng
dc.titlePapel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomolecularesspa
dc.title.translatedRole of IFN-λ in the pathogenesis of Systemic Lupus Erythematosus: biomolecular Mechanismseng
dc.type.driverinfo:eu-repo/semantics/article
dc.type.spaArtículo científico
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