Complement is a critical element of innate immunity, protecting individuals from a wide variety of microbial infections. This group of proteins is responsible for many features of in flammation and tissue damage. Because of its ability to mediate autoimmune tissue damage and to destroy host tissues, it is under tight regulation with many circulating and cell-membrane-bound complement regulatory proteins. The function of much of the circulating immunoglobulin has never been defined. We have advanced the hypothesis that one function of circulating immunoglobulin is to down-regulate complernent attack on host tissues in the presence of anti-self antibody. The data to support this hypothesis are reviewed. The data are consistent with the suggestion that one mechanism of action of intravenous immunoglobulin, used to treat patients with a variety of autoimmune diseases, is prevention of complement-mediated attack on host tissues.