Papel del IFN-λ en la patogénesis del Lupus eritematoso sistémico: mecanismos Biomoleculares
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Fecha
2024
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
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Sociedad Paraguaya de Reumatología
Resumen
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.
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.
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.
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Palabras clave
Autoinmunidad, Interferones, Lupus eritematoso sistémico, Receptores Interferón, Receptores tipo Toll
