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Academia Mexicana de Neurología, A.C.

2005, Número 5

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Rev Mex Neuroci 2005; 6 (5)


Mimetismo molecular en la neuropatogénesis del síndrome de Guillain-Barré

Ortega-Martínez MG, Jaramillo-Rangel G, Ancer-Rodríguez J, Trujillo JR

Idioma: Español
Referencias bibliográficas: 60
Paginas: 440-447
Archivo PDF: 91.66 Kb.


RESUMEN

El síndrome de Guillain-Barré (SGB) es la neuropatía autoinmune más común. Clínicamente se caracteriza por parálisis flácida, aguda y ascendente, que generalmente es precedida por una infección viral o bacteriana. El Campylobacter jejuni y el citomegalovirus (CMV) son los agentes patógenos encontrados con más frecuencia en las infecciones que anteceden a esta enfermedad. La infección por el virus de la inmunodeficiencia (VIH) puede complicarse con un SGB, que usualmente ocurre antes del desarrollo del SIDA. El SGB asociado al VIH se ha convertido en un gran problema, y no está muy claro si se relaciona con la misma infección por el VIH o a la reactivación de otros virus como el CMV. El mimetismo molecular entre componentes microbianos y del hospedero es el mecanismo responsable de la respuesta inmune humoral y celular involucrada en la neuropatogénesis del SGB y de otras enfermedades autoinmunes postinfecciosas. En esta revisión analizamos el papel del mimetismo molecular como el mecanismo causal del SGB.


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