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IRF-7 es el regulador maestro de las respuestas inmunes dependientes de interferón tipo I
Kenya Honda1, Hideyuki Yanai, Hideo Negishi
1Department of Immunology, Graduate School of Medicine and Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.
Nature
|April 1, 2005
Resumen
El factor de transcripción IRF-7 es esencial para las respuestas del interferón tipo I (IFN-alfa/beta) contra las infecciones virales. IRF-7 controla tanto la inmunidad innata como la adaptativa mediante la regulación de las vías de inducción de IFN.
Área de la Ciencia:
- Inmunología Inmunología.
- Virología Virología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- Los interferones de tipo I (IFN-alfa/beta) son cruciales para la inmunidad antiviral.
- Las respuestas IFN pueden ser desencadenadas por la detección viral citosólica o por la señalización del receptor 9 de tipo Toll (TLR9).
- La proteína del adaptador MyD88 está involucrada en la inducción de IFN mediada por TLR.
Objetivo del estudio:
- Investigar el papel del factor de transcripción IRF-7 en la inducción del gen IFN-alfa/beta.
- Determinar la necesidad de IRF-7 en las vías IFN independientes de MyD88 y dependientes de MyD88.
- Para aclarar la función de IRF-7 en las respuestas de las células dendríticas plasmocitoides y la inmunidad adaptativa.
Principales métodos:
- Se utilizaron ratones con deficiencia genética (Irf7-/- y Myd88-/-).
- Se evaluó la inducción del gen IFN-alfa/beta en los fibroblastos y los niveles séricos de IFN en ratones.
- Se evaluó la producción de IFN en las células dendríticas plasmocitoides y las respuestas de las células T CD8+.
Principales resultados:
- La IRF-7 es esencial para la inducción del gen IFN-alfa/beta a través de vías activadas por el virus (independientes de MyD88) y activadas por TLR (dependientes de MyD88).
- Los ratones Irf7-/- exhiben una mayor vulnerabilidad a las infecciones virales en comparación con los ratones Myd88-/- con niveles reducidos de IFN en suero.
- La robusta producción de IFN por la activación de TLR9 en las células dendríticas plasmocitoides es completamente dependiente de IRF-7, que rige las respuestas de las células T CD8+.
Conclusiones:
- IRF-7 es un regulador maestro que controla todos los aspectos de las respuestas de interferón de tipo I.
- La IRF-7 es crítica tanto para la inmunidad antiviral innata sistémica como para las respuestas inmunitarias adaptativas mediadas por las células dendríticas plasmocitoides.
- La vía MyD88-IRF-7 es fundamental para la producción de IFN inducida por TLR9 y la posterior inmunidad de las células T.
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