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Resumen
Una característica del sistema inmunitario de los animales vertebrados es su capacidad para mantener un equilibrio entre la reactividad y la quiescencia. Gracias a la descripción y al análisis de varios sistemas de receptores activadores e inhibidores, de células linfoides y mieloides, se ha postulado que los pares de receptores activadores e inhibidores son necesarios para iniciar, amplificar y terminar las respuestas inmunitarias. La importancia de este sistema regulador se ha puesto de manifiesto al observar una mayor susceptibilidad para desarrollar patología o fenómenos autoinmunes en cepas de ratones deficientes en algunos de estos receptores. En la artritis reumatoide, la inflamación crónica está causada por la interrelación entre infiltrados linfocitarios, macrófagos y fibroblastos sinoviales. Todas estas células expresan varios de estos receptores activadores y/o inhibidores. Algunos datos sugieren que una disfunción de algunos de estos receptores podría promover la inflamación crónica en la artritis reumatoide y posiblemente en otras enfermedades autoinmunes.
Palabras clave:
Receptor
HLA
Artritis reumatoide
Abstract
A hallmark of the vertebrate immune system is its ability to maintain a equilibrium between the extremes of reactivity and quiescence. With the detailed description and analysis of several inhibitory and activatory receptor systems on lymphoid and myeloid cells, a central paradigm has emerged in which the pairing of activation and inhibition is necessary to initiate, amplify, and then terminate immune responses. The importance of this regulation is demostrated by the autoimmunes disorders observed in mice with targeted disruption of inhibitory receptors. The self-perpetuating pathology in rheumatoid arthritis is caused by the interplay between lymphocytic infiltrates, synovial macrophages and fibroblasts, and their respective products. All of these cells express some of these receptors. Some datas suggests that a dysregulation of these systems may cause autoreactive stimulation in these cells, thus promoting the chronic inflammation in rheumatoid arthritis and possibly other autoimmune diseases.
Key words:
Receptor
MHC
Rheumatoid arthritis
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