Información del artículo
Hasta hace poco tiempo se consideraba que las células B tenían un papel secundario en la patogenia de la artritis reumatoide, limitado a la producción de autoanticuerpos. Sin embargo, la sorprendente buena respuesta clínica que la depleción sistémica de las células B ha demostrado en ensayos clínicos controlados y aleatorizados con pacientes con artritis reumatoide ha revitalizado el interés por el papel del linfocito B en la patogenia de esta enfermedad autoinmunitaria. Diversas evidencias indican que las células B pueden regular el curso de la respuesta inmunitaria mediante mecanismos alternativos no dependientes de la producción de anticuerpos. Estos mecanismos incluyen la presentación de antígenos y la liberación de factores solubles como citocinas proinflamatorias, metaloproteasas y quimiocinas. En esta revisión se resumen los datos experimentales que indican que la célula B participa en la patogenia de la arthritis reumatoide mediante un mecanismo multifactorial.
Palabras clave:
Linfocito B
Artritis reumatoide
Patogenia
Classically, B-cells have been considered to play a secondary role in the pathogenesis of rheumatoid artritis, restricted to the production of auto-antibodies. Nevertheless, the unexpected good clinical response that the systemic depletion of B-cells has demonstrated in a well-controlled clinical trial in patients with rheumatoid artritis has revitalized the interest in this cell type in the pathogenesis of this autoimmune disease. Several evidences suggest that B-cells can regulate the course of the immune response through antibody productionindependent mechanisms. These mechanisms include antigen presentation and the release of soluble factors such as proinflammatory cytokines, metalloproteinases, and chemokines. This article reviews experimental data supporting that the participation of B-cells in the pathogenesis of rheumatoid arthritis occurs through multiple mechanisms.
Keywords:
B-Lymphocites
Rheumatoid arthritis
Pathogenesis
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