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2014, Número 4

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Gac Med Mex 2014; 150 (4)


El factor de necrosis tumoral α (TNF-α) en las enfermedades autoinmunes (EA): biología molecular y genética

Fragoso JM, Vargas AG, Jiménez MS, Reyes HOD, Ramírez BJ

Idioma: Español
Referencias bibliográficas: 114
Paginas: 334-344
Archivo PDF: 173.16 Kb.


RESUMEN

Las enfermedades autoinmunes (EA) afectan aproximadamente al 5-8% de los individuos que viven en EE.UU., y representan un serio problema de salud pública a nivel global. Las EA crónicas se caracterizan por la pérdida de la tolerancia inmunológica a antígenos propios. Las consecuencias clínicas pueden ser desde leves hasta muy graves, llegando a afectar a uno o varios órganos blanco. Cinco de las EA más comunes son la artritis reumatoide (AR), el lupus eritematoso sistémico (LES), la enfermedad de Graves (EG), la diabetes mellitus de tipo 1 (DMt1) y la esclerosis múltiple (EM). Diversos estudios han documentado que el gen TNF-α y su producto proteico, el TNF-α (una potente citocina pleiotrópica con múltiples funciones celulares), juegan un papel fundamental en el inicio, desarrollo, susceptibilidad, gravedad y respuesta al tratamiento en diversas EA. El uso de terapias con anticuerpos monoclonales dirigidos contra el TNF-α ha dado resultados muy alentadores en AR y artritis reumatoide juvenil (ARJ), no así en LES o EM. Esta revisión presenta el papel biológico que juega el TNF-α en condiciones normales y patológicas (inicio, progresión, susceptibilidad, gravedad y respuesta al tratamiento) en la AR, el LES, la EG, la DMt1 y la EM.


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