IL-10 was originally described as a cytokine produced by Th2 cells and mediating antiinflammatory effects, by acting primarily on phagocytic cells and on antigen-presenting cells (1). IL-10 inhibits, in these cells, transcription and production of proinflammatory cytokines, such as TNF and IL-12, expression of MHC class II, and costimulatory molecules, as well as the production of reactive oxygen and nitrogen intermediates (1). In part through inhibition of IL-12 production and of costimulatory molecule expression on antigen-presenting cells, IL-10 has an overall suppressive effect on the generation of Th1 responses. In addition, IL-10 profoundly affects the bactericidal activity of phagocytic cells, allowing intracellular survival of pathogens such as Mycobacterium tuberculosis (2) and Leishmania major (3). In addition to inhibit the intracellular bactericidal mechanisms, IL-10 was shown to prevent TNF-mediated apoptosis of M. tuberculosis infected macrophages thus possibly facilitating the maintenance of a chronic infection (4). Many experimental and clinical studies have shown that the in vivo production of IL-10 during intracellular pathogen infections represents a regulatory mechanism to prevent pathogenic systemic inflammatory responses. Even in the presence of IL-10, the protective effect of a regulated Th1 response is largely preserved, although in some instances sterile cure in chronic infection by intracellular parasites may be prevented. Several studies also indicate that the principal source of IL-10 may be T cells that also produce IFN-, in addition or instead of Th2 cells or cells infected or exposed to parasite products, eg, macrophages, which may be the predominant producer of IL-10 during the early acute phases of the infection.