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La base estructural de la detección de la flagelina por NAIP5: una estrategia para limitar la evasión inmune del

Jeannette L Tenthorey¹, Nicole Haloupek¹, José Ramón López-Blanco²

¹Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.

Science (New York, N.Y.)

|November 18, 2017

Resumen

Este estudio revela cómo el inflamatorio flagellin-NAIP5-NLRC4 es activado por la flagelina bacteriana. Esta visión estructural de la activación de la proteína de repetición rica en leucina (NLR) del dominio de unión de nucleótidos por los ligandos proporciona una base para comprender los mecanismos de defensa del huésped.

Área de la Ciencia:

La inmunidad innata
Biología estructural
Microbiología

Sus antecedentes:

Las proteínas de repetición ricas en leucina (NLR) del dominio de unión de nucleótidos son sensores inmunológicos innatos citosólicos cruciales.
Comprender la base estructural de la activación de NLR por los ligandos es esencial para la defensa del huésped contra los patógenos.
NAIP5 (familia NLR, proteína inhibidora de la apoptosis 5) y NLRC4 forman un complejo inflamatorio al unirse a la flagelina bacteriana.

Objetivo del estudio:

Determinar la base estructural de la activación del NLR inducida por el ligando.
Elucidar el mecanismo por el cual la flagelina activa el inflamatorio NAIP5-NLRC4.

Principales métodos:

Se utilizó la crio-microscopía electrónica (cryo-EM) para determinar la estructura del inflamatorio NAIP5-NLRC4 ensamblado.
El análisis estructural se centró en las interacciones entre los dominios NAIP5 y la flagelina.

Principales resultados:

Se resolvió la estructura inflamatoria del flagellin-NAIP5-NLRC4 de aproximadamente 1,4 megadaltones.
Se observaron seis dominios NAIP5 que interactúan con múltiples regiones conservadas de flagelina.
Estas interacciones inducen una conformación abierta y activa de NAIP5, lo que demuestra cómo la unión del ligando activa un NLR.

Conclusiones:

El reconocimiento inmune innato de múltiples superficies de ligandos es una estrategia clave para la activación de NLR.
Este mecanismo de reconocimiento multiligando limita la evolución del patógeno y la evasión inmune.
Los hallazgos proporcionan información estructural crítica sobre la inmunidad innata mediada por NLR.

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