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Los controles de señalización MyD88 controlan la inducción de la miocarditis autoinmune
René R Marty1, Stephan Dirnhofer, Nora Mauermann
1Division of Experimental Critical Care Medicine, Department of Research, University Hospital, Basel, Switzerland.
Circulation
|January 13, 2006
Resumen
La señalización de MyD88 en las células dendríticas es crucial para iniciar la miocarditis autoinmune. El bloqueo de esta vía en las células presentadoras de antígenos puede prevenir la autoinmunidad específica del corazón y la cardiomiopatía.
Área de la Ciencia:
- Inmunología Inmunología.
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
- La autoinmunidad es autoinmunidad.
Sus antecedentes:
- La miocarditis autoinmune experimental (EAM) es un modelo de células T CD4+ para la cardiomiopatía posviral.
- La respuesta primaria de diferenciación mieloide 88 (MyD88) es esencial para la señalización del receptor tipo Toll y del receptor IL-1.
- La función específica de MyD88 en la patogénesis de la miocarditis sigue sin estar clara.
Objetivo del estudio:
- Investigar el papel de MyD88 en el desarrollo de la miocarditis autoinmune experimental.
- Determinar la fuente celular de la señalización de MyD88 crítica para la inducción de enfermedades.
Principales métodos:
- Se utilizaron ratones MyD88 deficientes (MyD88(-/-)) y de tipo salvaje (MyD88(+/+).
- Los ratones inmunizados con el péptido de cadena pesada alfa-miosina (MyHC-alfa) para inducir la EAM.
- Se evaluó la expansión de las células T CD4 +, la función de las células dendríticas (DC) y la producción de citoquinas.
Principales resultados:
- Los ratones MyD88(-/-) estaban protegidos de la EAM, mostrando una reducción de la expansión de las células T CD4 + específicas del corazón.
- Las células dendríticas MyD88(-/-) exhibieron una disminución de la capacidad de iniciación de las células T debido a la liberación defectuosa del factor de necrosis tumoral alfa.
- La restauración de la señalización de MyD88 en DCs restableció completamente la expansión de las células T y la miocarditis en ratones MyD88 ((-/-)).
Conclusiones:
- La señalización de MyD88 dentro de las células presentadoras de antígenos en los compartimentos periféricos es esencial para el desarrollo de la miocarditis autoinmune.
- Dirigirse a la señalización de MyD88 en estas células ofrece una estrategia potencial para prevenir la autoinmunidad y la cardiomiopatía específicas del corazón.
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