title: Complement determinations in human disease.
abstract: OBJECTIVE
  To define techniques used for complement measurements and examine the clinical relevance of alterations of complement determinations in disease.
  
  
  METHODS
  Data have been assembled from the authors' research, original articles, and reviews, as well as chapters and complete books on complement.
  
  
  METHODS
  Studies were chosen for inclusion by the opinions of the authors, relevant complement reviews, publications, and books.
  
  
  RESULTS
  Complement has been shown to possess approximately 31 proteins, some of which are enzymes (C1r, C1s, C2, factor B, factor D), some cofactors, some inhibitors or inactivators, and others composed of membrane-integrated proteins. All of the complement proteins have been purified, and many of the respective genes have been identified. The complement cascade is a dual-edged sword, causing protection against bacterial and viral invasion by promoting phagocytosis and inflammation. Pathologically, complement can cause substantial damage to blood vessels (vasculitis), kidney basement membrane and attached endothelial and epithelial cells (nephritis), joint synovium (arthritis), and erythrocytes (hemolysis) if it is not adequately controlled.
  
  
  CONCLUSIONS
  Definitive evidence is available that complement-mediated tissue destruction occurs after immune complex injury in the kidney and lung and may be important in lupus erythematosus and adult respiratory distress syndrome. Future studies on complement receptor structure and function may provide clues to treat effectively lupus, hemolytic anemias, and nephritis. In addition, gene therapy and antibody therapy need further refinement to treat immunodeficiency diseases.
authors.affiliation: Huntington Medical Research Institute, Pasadena, California, USA. yksvolg@caltech.edu
authors.forename: M Michael
authors.initials: MM
authors.lastname: Glovsky
authors.forename: Peter A
authors.initials: PA
authors.lastname: Ward
authors.forename: Kent J
authors.initials: KJ
authors.lastname: Johnson
mesh_terms: D003165:Complement System Proteins / Q000032:analysis / Q000172:deficiency; D006801:Humans; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D003165:Complement System Proteins