Doníz-Viveros AD, Copca-Barrientos M, Hernández-Uribe PS, Ortega-Espinosa JVA

Idioma: Ingles.
Referencias bibliográficas: 30
Paginas: 42-53
Archivo PDF: 271.45 Kb.

RESUMEN

La vasculitis IgA (HSP, por sus siglas en inglés) y el lupus eritematoso sistémico (SLE, por sus siglas en inglés) son enfermedades inmunológicas que podrían estar más interrelacionadas de lo que se piensa. La HSP es una enfermedad caracterizada por vasculitis sistémica de pequeños vasos y depósitos mesangiales de inmunoglobulina A, lo que conduce a fallas en el aclaramiento apoptótico y a la generación de un síndrome linfoproliferativo crónico. El SLE es una enfermedad caracterizada por una inflamación sistémica crónica que afecta múltiples órganos y sistemas, su origen radica en la formación de anticuerpos anti-DNA de doble cadena, que también son generados por fallas en el aclaramiento apoptótico. La HSP puede considerarse como un factor desencadenante de SLE, probablemente como resultado de alteraciones en el aclaramiento apoptótico, que podría estar relacionado con la inhibición de genes de ARN de cadena larga no codificante (ENST00000378432, ENST00000571370, uc001kfc.1 y uc010qna.2) en pacientes con HSP, que en consecuencia alteran el gen Fas (CD95), así como la función del factor de necrosis tumoral que a su vez inhibe la secreción de fosfatidilserina, lo que activaría los anticuerpos anti-DNA de doble cadena, el origen del SLE.

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