The complement system is an important factor in innate immunity. The third complement component, C3, is central to the classical, alternative and lectin pathways of complement activation. Activation products of the complement cascade contain neo-epitopes that are not present in the individual native components. Monoclonal antibodies detecting neo-epitopes have been used for direct quantification of activation at different steps in the complement cascade. The synthesis of C3 is tissue-specific and is modulated in response to a variety of stimulatory agents. An inherited deficiency of C3 predisposes the person to frequent assaults of bacterial infections. Proteolysis by certain enzymes results in the cleavage of C3 into C3a and C3b. C3a is a mediator of local inflammatory processes. C3a does induce smooth muscle contraction, increases vascular permeability, and causes histamine release from mast cells and basophilic leukocytes.