The hallmark of interleukin-10 (IL-10) is its capacity to inhibit cytokine synthesis and downregulate a cellular immune response. Originally identified as a T helper 2 (Th2) cytokine [1], IL-10 has been increasingly recognized to play a much broader role in the regulation of immune function. IL-10 is a pleiotropic cytokine with diverse effects on a variety of cell types [reviewed in 2, 3]. It suppresses Th1-dependent cellular immune responses and supports Th2-dependent antibody-mediated immune responses. IL-10 inhibits the capacity of macrophages to synthesize proinflammatory cytokines and other mediators and serves as part of an endogenous feedback loop to restrain inflammatory stimuli.

Cytokine networks are pivotal in the pathogenesis of rheumatoid arthritis (RA). IL-10 is expressed by macrophages and T cells in the rheumatoid synovium [4]. While inhibitory, the levels of IL-10 are presumably inadequate to control joint inflammation. The inflammatory response is launched into overdrive by proinflammatory cytokines such as tumor necrosis factor (TNF)-and IL-1 [5]. The vital role played by these proinflammatory cytokines in joint inflammation has been confirmed in clinical trials which show that TNF-blockade and, to a lesser extent, IL-1 antagonism reduce the signs and symptoms of RA [6–11]. The administration of IL-10 has a similar therapeutic potential through its ability to suppress the production of proinflammatory cytokines.