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La infección rompe la tolerancia de las células T
M Röcken1, J F Urban, E M Shevach
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Nature
|September 3, 1992
Resumen
La infección por Nippostrongylus brasiliensis puede romper la tolerancia de las células T establecida por la enterotoxina B (SEB) de Staphylococcus. Esto sugiere que los agentes infecciosos pueden desencadenar enfermedades autoinmunes mediante la activación de las células T anérgicas.
Área de la Ciencia:
- Inmunología Inmunología.
- La autoinmunidad es autoinmunidad.
- Enfermedad Infecciosa Enfermedad Infecciosa.
Sus antecedentes:
- La tolerancia de las células T, establecida a través de la deleción clonal o anergia, previene las respuestas autoinmunes.
- Las células T autorreactivas son normalmente suprimidas para mantener la auto-tolerancia.
Objetivo del estudio:
- Investigar si una infección concomitante puede romper la tolerancia establecida a las células T.
- Determinar el mecanismo por el cual los agentes infecciosos podrían eludir la tolerancia de las células T.
Principales métodos:
- Inducción de la tolerancia de las células T en ratones utilizando la enterotoxina B (SEB) de Staphylococcus.
- Desafiar las células T tolerantes in vitro con SEB para evaluar la producción de citoquinas (interleucina-2, interleucina-4).
- Infectar ratones tolerantes con el nematodo Nippostrongylus brasiliensis y analizar las respuestas de las células T in vivo.
Principales resultados:
- Las células T tolerantes a la SEB no produjeron interleucina-2 o -4 en el desafío de la SEB in vitro.
- La infección por N. brasiliensis en ratones tolerantes a la SEB condujo a una expansión normal de las células T tolerantes.
- La infección también dio lugar a un aumento de las células T que producen interleucina-4 y reaccionan a la SEB en animales tolerantes y normales.
Conclusiones:
- La infección por Nippostrongylus brasiliensis efectivamente elude la tolerancia de las células T inducidas por la SEB.
- Los agentes infecciosos pueden iniciar la autoinmunidad mediante la activación de las células T anérgicas a través de vías alternativas.
- Este estudio pone de relieve un mecanismo potencial para los desencadenantes infecciosos en el desarrollo de enfermedades autoinmunes.
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