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Una proteína del virus del herpes simplex citosólico inhibe la presentación de antígenos a los linfocitos T CD8+ T
I A York1, C Roop, D W Andrews
1Department of Pathology, McMaster University Hamilton, Ontario, Canada.
Cell
|May 20, 1994
Resumen
El virus del herpes simple (VHS) evadía la detección inmune al bloquear el reconocimiento de los linfocitos T citotóxicos (CTL). La proteína viral ICP47 impide que las células infectadas presenten péptidos virales en las moléculas de clase I del MHC, inhibiendo así la lisis mediada por CTL.
Área de la Ciencia:
- Inmunología Inmunología.
- Virología Virología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- El virus del herpes simple (VHS) infecta los fibroblastos humanos, lo que lleva a la resistencia contra los linfocitos T citotóxicos CD8 + (CTL).
- Las CTL normalmente reconocen los péptidos virales presentados por las proteínas de clase I del complejo mayor de histocompatibilidad (MHC) en las superficies celulares infectadas.
- La infección por HSV interrumpe este proceso de reconocimiento, permitiendo al virus evadir la vigilancia inmune.
Objetivo del estudio:
- Investigar el mecanismo por el cual las células infectadas por HSV evaden la lisis mediada por CD8+ y CTL.
- Para identificar el componente viral responsable de bloquear la presentación de antígenos virales.
- Para entender cómo la infección por HSV afecta la respuesta inmune del huésped.
Principales métodos:
- Infección de los fibroblastos humanos con el HSV.
- Análisis de la localización de proteínas de MHC clase I y la carga de péptidos dentro de las células infectadas.
- Evaluación de la lisis mediada por CD8+ CTL de las células infectadas.
- Investigación del papel de la proteína inmediata y temprana del VHS ICP47.7.
Principales resultados:
- Dentro de las 3 horas de la infección por HSV, los complejos de proteínas de clase I del MHC se retienen en el retículo endoplasmático / cis Golgi.
- Estos complejos MHC de clase I retenidos carecen de péptidos antigénicos, lo que los hace indetectables para las CTL.
- La proteína ICP47 del HSV es necesaria y suficiente para bloquear el transporte de MHC clase I e inhibir la lisis de CD8+ CTL.
- ICP47 parece interferir con la producción, estabilización o translocación de péptidos en el ER/cis Golgi.
Conclusiones:
- El HSV utiliza la proteína ICP47 para evadir activamente la detección de los linfocitos T CD8+.
- Este mecanismo de evasión implica la retención de complejos de MHC clase I en el ER/cis Golgi, evitando la presentación de péptidos antigénicos.
- La capacidad del HSV para inhibir las respuestas CTL CD8+ puede explicar el predominio observado de las CTL específicas del HSV CD4+ in vivo.
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