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Suicidio autocrino de células T mediado por APO-1/(Fas/CD95)
Nature
|February 2, 1995
Resumen
La activación del receptor de células T desencadena la apoptosis mediada por APO-1 (también conocida como Fas/CD95) en las células T humanas. Esta vía, que involucra al ligando APO-1, explica la deleción de las células T y la regulación de la respuesta inmune.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
Sus antecedentes:
- El receptor APO-1/(Fas/CD95), parte de la superfamilia de receptores TNF, es el mediador de la muerte celular programada (apoptosis).
- Las células T activadas (ATC) de ratones lpr / lpr muestran una apoptosis inducida por el receptor de células T defectuoso (TCR), lo que sugiere el papel de APO-1.
Objetivo del estudio:
- Para investigar la participación del receptor APO-1 en la apoptosis inducida por TCR en las células T humanas.
- Para aclarar el mecanismo de la apoptosis inducida por TCR y su regulación.
Principales métodos:
- Utilizó células Jurkat malignas, un clon de células T aloreactivas (S13) y ATC periférico.
- Se activa la señalización TCR utilizando anticuerpos anti-CD3 inmovilizados y la enterotoxina B (SEB) de Staphylococcus.
- Se evaluó la inhibición de la apoptosis utilizando fragmentos de anticuerpos anti-APO-1 y señuelos solubles del receptor APO-1.
Principales resultados:
- La activación de TCR indujo la expresión del ligando APO-1 y la apoptosis en todas las células T humanas probadas.
- La apoptosis fue inhibida significativamente al bloquear las interacciones de APO-1.
- Se detectó un ligando APO-1 soluble en el supernatante de las células Jurkat activadas.
Conclusiones:
- La apoptosis inducida por TCR en ATC puede ocurrir a través de la señalización autocrina mediada por ligando APO-1 (suicidio).
- Este mecanismo contribuye a la supresión de la respuesta inmune y la tolerancia periférica a través de la deleción de células T.
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