Finally, Baldwin et al. [44] recently showed that DCs derived from RA patients after therapy with either the soluble TNF receptor (TNFR) p55 Ig fusion protein, etanercept or the chimeric anti-TNFα monoclonal antibody infliximab showed impaired up-regulation of CD80 and CD86 after stimulation with lipopolysaccharide in vitro as well as poor T-cell stimulatory activity. The gene discussed is TNFRSF1A; the disease is rheumatoid arthritis.