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Respuesta anómala tipo 17 a la infección viral por células T CD8+ que carecen de T-bet y eomesodermina

Andrew M Intlekofer¹, Arnob Banerjee, Naofumi Takemoto

¹Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.

Science (New York, N.Y.)

|July 19, 2008

Resumen

Los factores de transcripción T-bet y eomesodermina (Eomes) son cruciales para que las células T CD8+ se conviertan en asesinos citotóxicos contra los patógenos intracelulares. Sin ellos, las células T CD8 + promueven la inflamación dañina en lugar de una defensa viral efectiva.

Área de la Ciencia:

Inmunología Inmunología.
Biología celular Biología celular.
Virología Virología.

Sus antecedentes:

Las células T CD8+ son críticas para el control de las infecciones por patógenos intracelulares.
Las células T CD8+ citotóxicas eliminan las células infectadas y secretan citoquinas.
Las vías de diferenciación de las células T CD8 + son clave para la defensa del huésped.

Objetivo del estudio:

Investigar el papel de los factores de transcripción T-bet y eomesodermina (Eomes) en la diferenciación de las células T CD8+ durante las infecciones virales.
Determinar las consecuencias de la falta de T-bet y Eomes para la respuesta inmune y la patología del huésped.

Principales métodos:

Análisis de la diferenciación de las células T CD8 + en ratones que carecen de T-bet y Eomes.
Modelo de infección utilizando el virus de la coriomeningitis linfocítica (LCMV).
Evaluación del compromiso del linaje de células T y las respuestas inflamatorias del huésped.

Principales resultados:

Las células T CD8 + deficientes en T-bet y Eomes no logran convertirse en asesinos citotóxicos.
Estas células se diferencian en un linaje secretor de interleucina-17, similar al ayudante T.
Los ratones que carecen de T-bet y Eomes en las células T desarrollan un síndrome inflamatorio severo caracterizado por la infiltración de neutrófilos.

Conclusiones:

T-bet y Eomes son esenciales para dirigir las células T CD8 + hacia una función efectiva de efector citotóxico contra los patógenos intracelulares.
La ausencia de estos factores conduce a la diferenciación aberrante de las células T CD8 +, promoviendo la inflamación perjudicial y la patología similar a la autoinmunidad.
Estos factores de transcripción aseguran el destino citotóxico apropiado de las células T CD8+ durante las infecciones virales.

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