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2012, Número 4

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Rev Cubana Hematol Inmunol Hemoter 2012; 28 (4)


Inmunopatogenia de la psoriasis. Impacto en las manifestaciones clínicas y el tratamiento de la enfermedad

Alfonso-Valdés ME

Idioma: Español
Referencias bibliográficas: 70
Paginas: 357-373
Archivo PDF: 92.56 Kb.


RESUMEN

La psoriasis es una enfermedad inflamatoria crónica de la piel mediada por células T que afecta a individuos con predisposición genética y presenta varios subtipos clínicos. Se caracteriza por la presencia de placas eritematosas bien definidas, escamosas y de bordes irregulares, que afectan fundamentalmente las regiones de los codos, las rodillas, el cuero cabelludo y el tronco. El alelo HLA-Cw6 del sistema principal de histocompatibilidad está relacionado con la presencia y severidad de la enfermedad. Desde el punto de vista fisiopatogénico, la psoriasis es una enfermedad inmune de tipo Th1, en la que es fundamental el eje IL-23/Th17. Las células Th17 producen las citocinas proinflamatorias (IL-17A, IL-17F, IL-22 e IL-26) que activan los queratinocitos y causan hiperproliferación y mayor producción de citocinas proinflamatorias y péptidos antimicrobianos, los que a su vez reclutan y activan otras células inmunes de la piel inflamada. Se produce así una amplificación de la respuesta inflamatoria que conduce a las manifestaciones clínicas de la enfermedad. El tratamiento de la psoriasis incluye agentes antiinflamatorios tópicos, fototerapia, inmunosupresores sistémicos y agentes biológicos, entre los que se encuentran las proteínas de fusión, los inhibidores del factor de necrosis tumoral alfa y los inhibidores de las interleucinas 12 y 23.


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