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El receptor nuclear huérfano RORgammat dirige el programa de diferenciación de las células ayudantes proinflamatorias
Ivaylo I Ivanov1, Brent S McKenzie, Liang Zhou
1Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, 540 First Avenue, New York, NY 10016, USA.
Cell
|September 23, 2006
Resumen
RORgammat se identifica como el factor de transcripción clave que impulsa el desarrollo de las células T ayudantes proinflamatorias 17 (Th17). Este descubrimiento destaca RORgammat como un objetivo terapéutico potencial para las enfermedades autoinmunes e inflamatorias.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología Molecular Biología Molecular
- Biología celular Biología celular.
Sus antecedentes:
- Las células T ayudantes 17 (Th17) son un linaje distinto de células T proinflamatorias.
- Las células Th17 son los principales contribuyentes a la patogénesis de las enfermedades autoinmunes.
- Los mecanismos moleculares que regulan la diferenciación de las células Th17 no se comprendieron completamente.
Objetivo del estudio:
- Para identificar el factor de transcripción clave responsable de la diferenciación de las células Th17.
- Para aclarar el papel de RORgammat en el desarrollo y la función de las células Th17.
- Explorar el potencial terapéutico de dirigirse a RORgammat en condiciones inflamatorias.
Principales métodos:
- Análisis de la expresión del factor de transcripción en las células T auxiliares.
- Análisis de la expresión génica de la IL-17 y la IL-17F.
- Estudios en ratones genéticamente modificados que carecen de RORgammat o IL-6.
- Evaluación de modelos de enfermedades autoinmunes.
Principales resultados:
- El receptor nuclear huérfano RORgammat fue identificado como el factor de transcripción clave para la diferenciación celular Th17.
- RORgammat induce la transcripción de los genes IL-17 e IL-17F en las células T ayudantes CD4 naïves.
- RORgammat es esencial para el desarrollo celular Th17 en respuesta a IL-6 y TGF-beta.
- Los ratones con deficiencia de RORgammat muestran una enfermedad autoinmune atenuada y carecen de células Th17 que se infiltran en los tejidos.
Conclusiones:
- RORgammat es un regulador crítico del compromiso y la diferenciación del linaje celular Th17.
- RORgammat juega un papel importante en la homeostasis inmunológica.
- RORgammat representa un objetivo terapéutico prometedor para las enfermedades autoinmunes e inflamatorias.
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