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Cbl-b regula la dependencia de CD28 de la activación de las células T
Y J Chiang1, H K Kole, K Brown
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA.
Nature
|January 26, 2000
Resumen
La molécula adaptadora Cbl-b regula la activación de las células T, ya que las células T que carecen de Cbl-b no necesitan coestimulación CD28 para la producción de interleucina-2. La deficiencia de Cbl-b restaura las respuestas de anticuerpos y aumenta la activación de Vav, lo que afecta la susceptibilidad a las enfermedades autoinmunes.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología Molecular Biología Molecular
- La señalización celular de las células.
Sus antecedentes:
- La activación de las células T requiere coestimulación a través del receptor de antígeno de células T (TCR) y CD28.
- La estimulación de la TCR por sí sola puede conducir a la anergia o eliminación de las células T, mecanismos de tolerancia inmune.
- La molécula adaptadora Cbl-b juega un papel en la regulación de las vías de señalización de las células T.
Objetivo del estudio:
- Investigar el papel de Cbl-b en la activación de las células T y la dependencia de CD28.
- Para determinar el impacto de la deficiencia de Cbl-b en las respuestas de las células T y la producción de anticuerpos.
- Explorar el vínculo entre la señalización Cbl-b y las enfermedades autoinmunes.
Principales métodos:
- Análisis de las células T deficientes en Cbl-b (Cbl-b(-/-)).
- Evaluación de la producción de interleucina-2 y las respuestas de anticuerpos dependientes de las células T en ratones sin Cbl-b y con deficiencia de CD28.
- Examen de las vías de señalización de TCR, incluidas las tirosinacinasas, Ras / MAPK, PLCgamma-1, movilización de Ca2 + y activación de Vav.
Principales resultados:
- Las células T deficientes en Cbl-b producían interleucina-2 sin coestimulación con CD28.
- La mutación Cbl-b-null restauró las respuestas de anticuerpos dependientes de las células T en ratones CD28-/-.
- Las vías de señalización de TCR como Zap-70, Lck, Ras / MAPK, PLCgamma-1 y Ca2 + no se vieron afectadas, pero la activación de Vav se mejoró en las células T Cbl-b(-/-) T.
Conclusiones:
- Cbl-b suprime selectivamente la activación de Vav mediada por TCR, lo que influye en la dependencia de CD28 en la activación de las células T.
- La desregulación de las vías de señalización moduladas por Cbl-b puede contribuir a enfermedades autoinmunes como la esclerosis múltiple.
- Cbl-b es un regulador crítico de la señalización de las células T y la tolerancia inmune.
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