Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
datacite.rights | http://purl.org/coar/access_right/c_abf2 | |
dc.contributor.author | Vergara Serpa, Oscar Vicente | |
dc.contributor.author | Apraez Mazabe, Nayla | |
dc.contributor.author | Córdoba Paredes, Juan Sebastián | |
dc.contributor.author | Arenas Contreras, Erika Jhohanna | |
dc.contributor.author | Lemus Arellano, Elva Rosa | |
dc.contributor.author | Herrera Olivares, Miguel Ángel | |
dc.contributor.author | Ruiz Pastrana, Geraldine Lucia | |
dc.contributor.author | Grajales Marín, Vanesa Alejandra | |
dc.contributor.author | Daza Arnedo, Rodrigo | |
dc.contributor.author | Vázquez Jiménez, Lourdes Carolina | |
dc.contributor.author | Rico Fontalvo, Jorge | |
dc.date.accessioned | 2024-07-03T22:16:55Z | |
dc.date.available | 2024-07-03T22:16:55Z | |
dc.date.issued | 2024 | |
dc.description.abstract | Introduction: 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.abstract | Introduction: 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.mimetype | ||
dc.identifier.doi | https://doi.org/10.18004/rpr/2024.10.01.37 | |
dc.identifier.issn | 24134341 (En línea) | |
dc.identifier.uri | https://hdl.handle.net/20.500.12442/14801 | |
dc.identifier.url | http://scielo.iics.una.py/scielo.php?script=sci_arttext&pid=S2413-43412024000100037&lng=es&nrm=iso&tlng=es | |
dc.language.iso | spa | |
dc.publisher | Sociedad Paraguaya de Reumatología | spa |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 United States | eng |
dc.rights.accessrights | info:eu-repo/semantics/openAccess | |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/us/ | |
dc.source | Revista Paraguaya de Reumatología | spa |
dc.source | Rev. parag. reumatol. | spa |
dc.source | Vol. 10 No. 1, (2024) | |
dc.subject | Autoinmunidad | spa |
dc.subject | Interferones | spa |
dc.subject | Lupus eritematoso sistémico | spa |
dc.subject | Receptores Interferón | spa |
dc.subject | Receptores tipo Toll | spa |
dc.subject.keywords | Autoimmunity | eng |
dc.subject.keywords | Interferons | eng |
dc.subject.keywords | Systemic lupus erythematosus | eng |
dc.subject.keywords | Interferon receptors | eng |
dc.subject.keywords | Toll-like receptors | eng |
dc.title | Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares | spa |
dc.title.translated | Role of IFN-λ in the pathogenesis of Systemic Lupus Erythematosus: biomolecular Mechanisms | eng |
dc.type.driver | info:eu-repo/semantics/article | |
dc.type.spa | Artículo científico | |
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