RESUMEN
Rheumatoid arthritis (RA) is a chronic inflammatory arthritis affecting 1% of the population. The immunologic dysfunction underlying this immune disorder is complex and intricate with the involvement of various immune cells as well as cytokines and surface molecules. While inhibition of TNF-alpha has changed the outlook of patients with this disorder, it regulates only one aspect of the inflammatory cascade associated with RA. This is corroborated by experience in the clinic, where a significant proportion of the patients do not have clinical benefit with such therapies. Furthermore, a number of patients experience blunting of the initial therapeutic benefits of TNF-alpha-targeted therapies. Thus, a different approach to regulate the immune dysfunction associated with RA is necessary. T cells are considered important in the pathogenesis of RA and abatacept, a fusion protein, was developed to abolish the activation of the T cell by blocking its interaction with the antigen-presenting cell. Abatacept has demonstrated promising clinical improvements in patients with RA. Although clinical experience with this new drug is limited and its mechanism of action remains to be understood, the data on the safety profile are reassuring.
