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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
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Degradación funcional: Un mecanismo de activación del inflamatorio NLRP1 por diversas enzimas patógenas
Andrew Sandstrom1,2, Patrick S Mitchell1, Lisa Goers3,4,5
1Division of Immunology and Pathogenesis, Department of Molecular & Cell Biology, and Cancer Research Laboratory, University of California, Berkeley, CA, USA.
Science (New York, N.Y.)
|March 16, 2019
Resumen
La toxina del ántrax activa los inflamatorios NLRP1B desencadenando su degradación. Este proceso mediado por el proteasoma libera un fragmento que activa la caspasa-1, revelando un mecanismo unificado para la activación del inflamasoma.
Área de la Ciencia:
- Inmunología
- Biología molecular
- Microbiología
Sus antecedentes:
- Los inflammasomas son los iniciadores clave de la inmunidad innata, mediando la activación de la caspasa-1.
- La activación del inflamatorio NLRP1B se desencadena por la escisión de la proteasa de la toxina letal del ántrax, pero el mecanismo sigue sin estar claro.
Objetivo del estudio:
- Para aclarar el mecanismo de activación del inflamatorio NLRP1B después de la escisión de la proteasa.
- Identificar vías conservadas para la activación de NLRP1B por efectores microbianos.
Principales métodos:
- Se investigó el papel de la degradación mediada por proteasomas en la activación de NLRP1B.
- Factores microbianos identificados que inducen la degradación y activación de NLRP1B mediante ensayos bioquímicos.
Principales resultados:
- La escisión de NLRP1B conduce a la degradación mediada por el proteosoma de sus dominios N-terminales.
- Esta degradación libera un fragmento C-terminal que activa potentemente la caspasa-1.
- Se identificó a *Shigella flexneri* IpaH7.8 como una ubiquitina ligasa que induce la degradación y activación de NLRP1B.
Conclusiones:
- La activación de NLRP1B es impulsada por la degradación mediada por el proteasoma, no solo por la escisión.
- Este mecanismo de degradación proporciona una vía unificada para la activación de NLRP1B por varias enzimas codificadas por patógenos.
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