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Microglía cerebelosa derivada de IL-17A mitiga los déficits conductuales y sinápticos relacionados con el autismo

Jun Yin¹, Wei Li¹, Li-Ping Shen^1,2

¹State Key Laboratory of Pharmaceutical Biotechnology, National Resource Center for Mutant Mice, Department of Anesthesiology, Nanjing Drum Tower Hospital, Institute for Brain Sciences, and Department of Physiology and AI Biology, School of Life Sciences, Nanjing University, Nanjing, China.

Molecular psychiatry

|February 9, 2026

Resumen

La interleucina-17A (IL-17A) derivada de microglía en el cerebelo es crucial para el comportamiento social en modelos de trastorno del espectro autista (TEA). La restauración de la señalización de IL-17A mejora los síntomas similares al TEA.

Área de la Ciencia:

Neurociencia
Inmunología
Genética

Sus antecedentes:

La interleucina-17 (IL-17) es una citoquina proveniente principalmente de las células T helper 17 periféricas.
El papel de la IL-17 originada en células del sistema nervioso central, particularmente en el cerebro, no se comprende bien.
El trastorno del espectro autista (TEA) es una afección del neurodesarrollo con factores genéticos y ambientales complejos.

Objetivo del estudio:

Investigar la función de la señalización de IL-17A en el cerebelo de un modelo de ratón para el TEA.
Determinar la fuente celular y los objetivos neuronales específicos de la IL-17A en el contexto del comportamiento social.
Explorar el potencial terapéutico de la modulación de la señalización de IL-17A para el TEA.

Principales métodos:

Se utilizaron ratones Fmr1-KO, un modelo genético para el TEA.
Se investigó la expresión y señalización de IL-17A en el cerebelo.
Se examinaron los efectos de la manipulación de IL-17A en la excitabilidad de las células de Purkinje (PC) y los comportamientos sociales.
Se administró IL-17A directamente y se indujo su liberación utilizando poli(I:C).

Principales resultados:

Se identificó una señalización aberrante de IL-17A en el cerebelo de ratones Fmr1-KO.
La IL-17A cerebelosa, producida exclusivamente por la microglía, regula los comportamientos sociales.
La IL-17A mantiene la excitabilidad neuronal y suprime la neurotransmisión inhibitoria en las células de Purkinje (PC) cerebelosas.
La disminución de la señalización del receptor de IL-17A en las PC mimetizó los déficits similares al TEA.
La administración de IL-17A o la inducción de su liberación restauraron la excitabilidad de las PC y mejoraron los síntomas similares al TEA.

Conclusiones:

La IL-17A derivada de microglía desempeña un papel crítico en el procesamiento social cerebeloso.
La señalización de IL-17A en las PC cerebelosas es esencial para la cognición social normal.
La modulación de la señalización de IL-17A presenta una vía terapéutica potencial para el TEA.

Palabras clave:

interleucina-17A microglía cerebelo trastorno del espectro autista comportamiento social neuronas de Purkinje excitabilidad neuronal neurotransmisión inhibitoria terapéutica

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