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La autofagia no canónica inhibe la respuesta autoinflamatoria parecida al lupus a las células moribundas
Jennifer Martinez1,2, Larissa D Cunha1, Sunmin Park3
1Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Nature
|April 21, 2016
Resumen
Los defectos en la fagocitosis asociada a LC3 (LAP), un proceso de aclaramiento celular, pueden causar una enfermedad similar al lupus eritematoso sistémico (LES). El deterioro de la LAP conduce a autoanticuerpos y daño renal, a diferencia de la autofagia canónica.
Área de la Ciencia:
- Inmunología
- Biología celular
- Patogénesis de las enfermedades autoinmunes
Sus antecedentes:
- El aclaramiento defectuoso de las células moribundas está implicado en la patogénesis del lupus eritematoso sistémico (LES).
- La fagocitosis asociada a LC3 (LAP) es una vía de autofagia no canónica crucial para la digestión de las células moribundas engullidas.
- Las predisposiciones genéticas para el LES se han relacionado con los genes involucrados tanto en la autofagia canónica como en la LAP.
Objetivo del estudio:
- Investigar las consecuencias in vivo de un LAP defectuoso en el desarrollo de fenómenos similares al LES.
- Diferenciar las funciones de LAP frente a la autofagia canónica en el aclaramiento de las células moribundas y la patogénesis de la enfermedad.
Principales métodos:
- Generación y análisis de ratones con deficiencia de componentes de la vía LAP.
- Evaluación de autoanticuerpos séricos, citoquinas inflamatorias y patología renal en ratones con deficiencia de LAP.
- Estudios in vivo que incluyen la inyección de células moribundas en ratones con deficiencia de LAP y de tipo salvaje.
Principales resultados:
- Los ratones que carecían de componentes de LAP exhibieron autoanticuerpos séricos elevados, citoquinas inflamatorias y daño renal.
- Las células moribundas engullidas se degradaron poco en ratones con deficiencia de LAP, lo que condujo a la liberación de citoquinas proinflamatorias.
- La administración repetida de células moribundas aceleró el desarrollo de la enfermedad similar al LES en ratones con deficiencia de LAP.
Conclusiones:
- Los defectos en la fagocitosis asociada a LC3 (LAP), no la autofagia canónica, pueden conducir a fenómenos similares al LES.
- La LAP alterada contribuye a la patogénesis del lupus eritematoso sistémico al interrumpir el aclaramiento de las células moribundas y promover la inflamación.
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