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Pérdida de la tolerancia de los islotes pancreáticos inducida por la expresión de las células beta de
N Sarvetnick1, J Shizuru, D Liggitt
1Department of Developmental Biology, Genentech, Inc., South San Francisco, California 94080.
Nature
|August 30, 1990
Resumen
La expresión de interferón-gamma (IFN-gamma) en el páncreas causa diabetes autoinmune al promover la destrucción mediada por linfocitos de los islotes pancreáticos. Este estudio muestra que IFN-gamma induce una pérdida de auto-tolerancia, lo que lleva a un ataque inmune en islotes normales.
Área de la Ciencia:
- Inmunología Inmunología.
- Endocrinología Endocrinología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- El interferón-gamma (IFN-gamma) es una citocina clave en las respuestas inmunes a las infecciones.
- Estudios previos establecieron que los ratones transgénicos que expresan IFN-gamma bajo el promotor de insulina (ins-IFN-gamma) desarrollan diabetes.
- Esta diabetes se caracteriza por la destrucción progresiva de los islotes pancreáticos debido a la infiltración de células inflamatorias.
Objetivo del estudio:
- Para aclarar los mecanismos inmunológicos específicos subyacentes a la diabetes autoinmune inducida por IFN-gamma.
- Para determinar si los linfocitos median la destrucción de los islotes pancreáticos en ratones ins-IFN-gamma.
- Para investigar el papel de IFN-gamma en la inducción de una pérdida de auto-tolerancia a las células de los islotes pancreáticos.
Principales métodos:
- Análisis de ratones ins-IFN-gamma para identificar los mediadores celulares de la destrucción de las islas.
- Injerto de islotes histocompatibles en ratones ins-IFN-gamma para evaluar la supervivencia de los islotes in vivo.
- En ensayos citotóxicos in vitro se utilizaron linfocitos de ratones ins-IFN-gamma contra islotes normales.
Principales resultados:
- La pérdida de células de islotes en ratones ins-IFN-gamma está mediada por linfocitos.
- Los islotes histocompatibles injertados fueron destruidos en los receptores transgénicos.
- Los linfocitos de ratones ins-IFN-gamma exhibieron citotoxicidad directa hacia islotes normales in vitro.
Conclusiones:
- La expresión pancreática de IFN-gamma puede romper la auto tolerancia a las células de los islotes.
- IFN-gamma actúa como un inductor de la actividad costimulatoria, crucial para la activación de los linfocitos.
- Estos hallazgos resaltan el papel de IFN-gamma en el inicio de respuestas autoinmunes contra los islotes pancreáticos.
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