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

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-...

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Autores:: Vergara Serpa, Oscar Vicente
Apraez Mazabe, Nayla
Córdoba Paredes, Juan Sebastián
Arenas Contreras, Erika Jhohanna
Lemus Arellano, Elva Rosa
Herrera Olivares, Miguel Ángel
Ruiz Pastrana, Geraldine Lucia
Grajales Marín, Vanesa Alejandra
Daza Arnedo, Rodrigo
Vázquez Jiménez, Lourdes Carolina
Rico Fontalvo, Jorge

Tipo de recurso:

Fecha de publicación:: 2024

Institución:: Universidad Simón Bolívar

Repositorio:: Repositorio Digital USB

Idioma:: spa

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dc.title.spa.fl_str_mv	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
dc.title.translated.eng.fl_str_mv	Role of IFN-λ in the pathogenesis of Systemic Lupus Erythematosus: biomolecular Mechanisms
title	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
spellingShingle	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares Autoinmunidad Interferones Lupus eritematoso sistémico Receptores Interferón Receptores tipo Toll Autoimmunity Interferons Systemic lupus erythematosus Interferon receptors Toll-like receptors
title_short	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
title_full	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
title_fullStr	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
title_full_unstemmed	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
title_sort	Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
dc.creator.fl_str_mv	Vergara Serpa, Oscar Vicente Apraez Mazabe, Nayla Córdoba Paredes, Juan Sebastián Arenas Contreras, Erika Jhohanna Lemus Arellano, Elva Rosa Herrera Olivares, Miguel Ángel Ruiz Pastrana, Geraldine Lucia Grajales Marín, Vanesa Alejandra Daza Arnedo, Rodrigo Vázquez Jiménez, Lourdes Carolina Rico Fontalvo, Jorge
dc.contributor.author.none.fl_str_mv	Vergara Serpa, Oscar Vicente Apraez Mazabe, Nayla Córdoba Paredes, Juan Sebastián Arenas Contreras, Erika Jhohanna Lemus Arellano, Elva Rosa Herrera Olivares, Miguel Ángel Ruiz Pastrana, Geraldine Lucia Grajales Marín, Vanesa Alejandra Daza Arnedo, Rodrigo Vázquez Jiménez, Lourdes Carolina Rico Fontalvo, Jorge
dc.subject.spa.fl_str_mv	Autoinmunidad Interferones Lupus eritematoso sistémico Receptores Interferón Receptores tipo Toll
topic	Autoinmunidad Interferones Lupus eritematoso sistémico Receptores Interferón Receptores tipo Toll Autoimmunity Interferons Systemic lupus erythematosus Interferon receptors Toll-like receptors
dc.subject.keywords.eng.fl_str_mv	Autoimmunity Interferons Systemic lupus erythematosus Interferon receptors Toll-like receptors
description	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.
publishDate	2024
dc.date.accessioned.none.fl_str_mv	2024-07-03T22:16:55Z
dc.date.available.none.fl_str_mv	2024-07-03T22:16:55Z
dc.date.issued.none.fl_str_mv	2024
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dc.type.spa.none.fl_str_mv	Artículo científico
dc.identifier.issn.none.fl_str_mv	24134341 (En línea)
dc.identifier.uri.none.fl_str_mv	https://hdl.handle.net/20.500.12442/14801
dc.identifier.doi.none.fl_str_mv	https://doi.org/10.18004/rpr/2024.10.01.37
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identifier_str_mv	24134341 (En línea)
url	https://hdl.handle.net/20.500.12442/14801 https://doi.org/10.18004/rpr/2024.10.01.37 http://scielo.iics.una.py/scielo.php?script=sci_arttext&pid=S2413-43412024000100037&lng=es&nrm=iso&tlng=es
dc.language.iso.none.fl_str_mv	spa
language	spa
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dc.publisher.spa.fl_str_mv	Sociedad Paraguaya de Reumatología
dc.source.spa.fl_str_mv	Revista Paraguaya de Reumatología Rev. parag. reumatol.
dc.source.none.fl_str_mv	Vol. 10 No. 1, (2024)
institution	Universidad Simón Bolívar
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spelling	Vergara Serpa, Oscar Vicente30a80973-5920-4b7a-84a1-fdb02358301d-1Apraez Mazabe, Naylafca588d2-9cfe-4b96-9e66-893d8597bf81-1Córdoba Paredes, Juan Sebastiánff89b059-754a-4d31-b538-884b50a6dd47-1Arenas Contreras, Erika Jhohanna5c9fdd7f-4b67-47ab-974b-e57cd29ab2c3-1Lemus Arellano, Elva Rosa1a4e6522-38ae-4b56-97c7-2bdff1a486d2-1Herrera Olivares, Miguel Ángel0711d1b6-57c5-4098-a943-d90db48043a3-1Ruiz Pastrana, Geraldine Lucia0e520fb8-8a82-49ab-bccb-f837f72ed59d-1Grajales Marín, Vanesa Alejandra01f9d051-bf08-4f2f-b209-aadb248b5125-1Daza Arnedo, Rodrigo82ba690f-f5de-45bc-bc67-5d2f7ca76c9f-1Vázquez Jiménez, Lourdes Carolina4793e5bb-f5b2-4dab-af82-7c97f78f765a-1Rico Fontalvo, Jorgea156782c-eb0d-4540-a7cb-92742ffaee75-12024-07-03T22:16:55Z2024-07-03T22:16:55Z202424134341 (En línea)https://hdl.handle.net/20.500.12442/14801https://doi.org/10.18004/rpr/2024.10.01.37http://scielo.iics.una.py/scielo.php?script=sci_arttext&pid=S2413-43412024000100037&lng=es&nrm=iso&tlng=esIntroduction: 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.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.pdfspaSociedad Paraguaya de ReumatologíaAttribution-NonCommercial-NoDerivs 3.0 United Stateshttp://creativecommons.org/licenses/by-nc-nd/3.0/us/info:eu-repo/semantics/openAccesshttp://purl.org/coar/access_right/c_abf2Revista Paraguaya de ReumatologíaRev. parag. reumatol.Vol. 10 No. 1, (2024)AutoinmunidadInterferonesLupus eritematoso sistémicoReceptores InterferónReceptores tipo TollAutoimmunityInterferonsSystemic lupus erythematosusInterferon receptorsToll-like receptorsPapel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos BiomolecularesRole of IFN-λ in the pathogenesis of Systemic Lupus Erythematosus: biomolecular Mechanismsinfo:eu-repo/semantics/articleArtículo científicohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_2df8fbb1Chyuan IT, Tzeng HT, Chen JY. Signaling Pathways of Type I and Type III Interferons and Targeted Therapies in Systemic Lupus Erythematosus. Cells. 2019; 8(9):963. DOI: https://doi. org/10.3390/cells8090963.Smith CD, Cyr M. The history of lupus erythematosus. From Hippocrates to Osler. Rheum Dis Clin North Am. 1988; 14(1):1-14. DOI: https://doi.org/10.1016/S0889-857X (21)00014-2.Duarte-García A, Hocaoglu M, Osei-Onomah SA, Dabit JY, Giblon RE, Helmick CG, et al. Population-based incidence and time to classification of systemic lupus erythematosus by three different classification criteria: a Lupus Midwest Network (LUMEN) study. Rheumatology. 2022; 61(6):2424-31. DOI: https://doi.org/10.1093/ rheumatology/keab879.Barber MRW, Drenkard C, Falasinnu T, Hoi A, Mak A, Kow NY, et al. Global epidemiology of systemic lupus erythematosus. Nat Rev Rheumatol. 2021; 17(9):515-32. DOI: https://doi.org/10.1038/ s41584-021-00608-9.Dall’Era M, Cisternas MG, Snipes K, Herrinton LJ, Gordon C, Helmick CG. 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DOI: https://doi.org/ 10.1177/0961203319865791.ORIGINALPDF.pdfPDF.pdfapplication/pdf396214https://bonga.unisimon.edu.co/bitstreams/068e2953-bb40-4be0-81dd-297aeb869964/download3fa7d9f01a23d94f0ce00965eca66305MD52CC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; charset=utf-8905https://bonga.unisimon.edu.co/bitstreams/84f25f83-6340-46ca-9cfc-6747e438b55e/download2f656a26de8af8c32aaacd5e2a33538cMD53LICENSElicense.txtlicense.txttext/plain; charset=utf-8381https://bonga.unisimon.edu.co/bitstreams/fe49f979-f71b-4ec8-87fc-ec5fce6fac78/download733bec43a0bf5ade4d97db708e29b185MD54TEXTArticulo Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico mecanismos Biomoleculares.txtArticulo Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico mecanismos Biomoleculares.txtExtracted texttext/plain49129https://bonga.unisimon.edu.co/bitstreams/6feddbad-bb6d-4690-b53b-1deaf4d86da6/download096483182e46709d73c427ef06bc23f5MD55PDF.txtPDF.txtExtracted texttext/plain49129https://bonga.unisimon.edu.co/bitstreams/21f529aa-c770-45cd-8a8b-b6307674e57b/download096483182e46709d73c427ef06bc23f5MD57PDF.pdf.txtPDF.pdf.txtExtracted texttext/plain49129https://bonga.unisimon.edu.co/bitstreams/9804673d-dc55-49bf-9c53-f7dc710585dc/download096483182e46709d73c427ef06bc23f5MD59THUMBNAILArticulo Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico mecanismos Biomoleculares.jpgArticulo Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico mecanismos Biomoleculares.jpgGenerated Thumbnailimage/jpeg4894https://bonga.unisimon.edu.co/bitstreams/79aaa439-89f0-424c-aacd-8070ae936784/downloadb45c9eb6833442714f280a227f8fea77MD56PDF.jpgPDF.jpgGenerated Thumbnailimage/jpeg4894https://bonga.unisimon.edu.co/bitstreams/6d657ae7-d740-435e-a91e-19e441801c37/downloadb45c9eb6833442714f280a227f8fea77MD58PDF.pdf.jpgPDF.pdf.jpgGenerated Thumbnailimage/jpeg4894https://bonga.unisimon.edu.co/bitstreams/6f510e77-2b13-4bf9-a776-634f513ad4e5/downloadb45c9eb6833442714f280a227f8fea77MD51020.500.12442/14801oai:bonga.unisimon.edu.co:20.500.12442/148012024-08-14 21:53:44.032http://creativecommons.org/licenses/by-nc-nd/3.0/us/Attribution-NonCommercial-NoDerivs 3.0 United Statesopen.accesshttps://bonga.unisimon.edu.coRepositorio Digital Universidad Simón Bolívarrepositorio.digital@unisimon.edu.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

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

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