Complement is a humoral defense system that protects the host from microorganisms by inducing an inflammatory reaction at the site of invasion. However, complement activation is not limited to microbial protection, but is generally activated in any tissue damage irrespective of the stimulus that initiated the reaction. Thus, complement is a double-edged sword which, when activated improperly, may contribute to inflammation and tissue damage. Weisman et al. demonstrated in 1990 that specific complement inhibition markedly reduced tissue damage in experimental myocardial infarction (1), a number of animal and clinical studies have documented that activation of complement contributes to the ischemia/reperfusion injury in general, and to the pathophysiology of various autoimmune diseases, trauma, systemic inflammatory response syndrome, septicemia, and transplant rejection (for review, see refs. 2–5).