Current understanding of the pathogenesis of rheumatoid arthritis has
provided evidence that therapeutic benefit can be achieved by using an
tagonists targeted to the inflammatory cytokines involved, mainly tumo
ur necrosis factor-alpha and interleukin-1. Gene delivery of antagonis
ts, which can inhibit the production or action of these cytokines and
other mediators, has been achieved in experimental animal models. This
new method of delivery can produce therapeutic effects at lower conce
ntrations and in a local environment, overcoming the adverse effects t
hat often accompany protein therapy. However, several technological an
d biological restraints preclude the immediate adaptation of this meth
od to human treatment. Based on the experimental evidence, possible ta
rget therapeutic genes, cell types and vector systems that could be us
ed are discussed in this article.