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Memoria de la inflamación en las células T reguladoras

Joris van der Veeken¹, Alvaro J Gonzalez², Hyunwoo Cho²

¹Howard Hughes Medical Institute and Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

|August 9, 2016

Resumen

Las células T reguladoras (Treg) mejoran su función supresora cuando se exponen a la inflamación, pero pierden esta potenciación con el tiempo. Este efecto de "menos memoria" previene la inmunosupresión prolongada de los desencadenantes inflamatorios repetidos.

Área de la Ciencia:

Inmunología
Biología celular
La epigenética

Sus antecedentes:

Las células T reguladoras (Treg) son cruciales para la regulación del sistema inmunológico.
Las células Treg pueden mejorar su función supresora al encontrarse con estímulos inflamatorios.
No se comprende bien la estabilidad a largo plazo de estos cambios funcionales en las células Treg.

Objetivo del estudio:

Investigar la estabilidad de los cambios inducidos por la inflamación en la función de las células Treg.
Determinar si las células Treg conservan una mayor capacidad supresora a largo plazo.
Comprender los mecanismos moleculares que subyacen a la memoria funcional de las células Treg.

Principales métodos:

Utilizó el rastreo genético inducible en células eucariotas.
Se analizaron los cambios transcripcionales y epigenómicos en las células Treg.
Capacidad supresora funcional evaluada de las células Treg a lo largo del tiempo.

Principales resultados:

Las células Treg experimentadas por la inflamación revirtieron muchos cambios transcripcionales y epigenómicos inducidos por la activación.
La función supresora mejorada de las células Treg disminuyó con el tiempo.
La población de células Treg demostró una falta de potenciación funcional estable a largo plazo.

Conclusiones:

La potenciación de las células Treg inducida por la inflamación es transitoria y reversible.
La naturaleza "sin memoria" de la potenciación de las células Treg previene la inmunosupresión sostenida.
Este mecanismo es vital para mantener la homeostasis inmune durante eventos inflamatorios repetidos.

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