Immune injury in the lung is classically divided into types I-IV hypersensitivity, with the complement system being involved in types II and III hypersensitivity. Anaphylaxis and asthma are generally considered prototypes of type I hypersensitivity and hypersensitivity pneumonitis as an example of type III hypersensitivity in the lung. However, in asthma, for example, increasing evidence indicates that in addition to mast cells, T lymphocytes play an important role. Therefore, considering asthma as strictly a type I mediated reaction is too simplistic. This report will review the evidence regarding the involvement of the complement system and complement activation products in anaphylaxis, asthma and immune complex disease in various experimental models of pulmonary disease. Identification of the mediators responsible for the symptoms may suggest rational targets for the continued development of effective therapy to combat immune injury in the lung.