In recent years, research in clinical immunology has focused on T and B cells, in view of the hypothesis that autoimmune disorders are antigen driven. Macrophages, in turn, while long recognized as playing an important role in chronic inflammatory disorders (1) including rheumatoid arthritis (RA), have only recently gained widespread attention, triggered by findings that monokines dominate the cytokine profile in inflammatory synovitis. In RA, activated macrophages are enriched in the rheumatoid synovium and are also found in strategic sites within the destructive pannus tissue (2, 3). In addition, macrophages and circulating monocytes spontaneously produce large amounts of prostanoids and/or proinflammatory cytokines (4-6), and peripheral blood monocytes show increased phagocytic activity (7). Several trials of conventional and experimental therapies, in turn, document with increasing clarity that whenever there is a marked clinical response, there are also signs of down-regulation of the mononuclear phagocyte system (5, 8, 9). From these observations, it may be deduced that before we find means to specifically