2003, Número 3
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Med Cutan Iber Lat Am 2003; 31 (3)
Expresión del antígeno linfocitario cutáneo en las placas alopécicas de pacientes con alopecia areata
Lacueva L, Hausmann G, Ferrando J
Idioma: Español
Referencias bibliográficas: 81
Paginas: 161-172
Archivo PDF: 562.39 Kb.
RESUMEN
El objetivo de este trabajo ha sido el análisis cualitativo y cuantitativo del infiltrado inflamatorio presente en las placas alopécicas de cuero cabelludo de pacientes con alopecia areata (AA), a nivel intraepidérmico, intrafolicular, perifolicular y perivascular, así como la expresión del antígeno linfocitario cutáneo “cutaneous lymphocyte antigen” (CLA) por las células de ese infiltrado, en esas mismas áreas.
Material y métodos: Para ello, hemos contado con 20 muestras de cuero cabelludo(cc): 12 obtenidas de la periferia de placas alopécicas de pacientes con diferentes formas clínicas de AA (en los casos de AA total y AA universal se tomaron de la región occipital) y 8 de individuos control aparentemente sanos.
Se realizó estudio inmunohistoquímico con los anticuerpos monoclonales[AcMo) anti-CD1a, anti-CD4, anti-CD8, anti-CD68 y HECA-452 (anti-CLA) según la técnica de la biotina-estreptoavidina-peroxidasa.
Resultados: Los resultados mostraron que la mayor celularidad correspondió a las placas de AA, a las áreas perifolicular y perivascular, donde observamos un 34% y 36% de las células del infiltrado respectivamente. El fenotipo predominante fue de linfocitos T cooperadores (CD4), que suponían el 41% del total de células. La relación linfocitos T CD4/CD8 fue 5,2. En cuanto a las secciones de cc sano, el predominio del infiltrado se observó a nivel intraepidérmico (51%). El 76% de ese infiltrado eran células de Langerhans y el cociente CD4/CD8 fue de 1,47.
Respecto a la expresión del CLA, el 29% de las células en las muestras de AA se tiñeron con HECA-452; es decir, fue casi seis veces superior a la expresión del CLA en las secciones de cc sano, en las que solo el 5% de las células fueron HECA-452 positivas.
Conclusión: Los datos obtenidos dan soporte a la hipótesis de que el CLA probablemente está implicado en la etiopatogenia de la AA, posiblemente favoreciendo los movimientos migratorios de las células inmunocompetentes de la piel, secundarios a la manifestación autoantígeno.
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