Complement activation following oxidative stress

• Published in: Molecular immunology Vol. 36; no. 13; pp. 941 - 948
• Main Authors: Collard, C.D, Lekowski, R, Jordan, J.E, Agah, A, Stahl, G.L
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.09.1999
• Subjects: Animals; Complement; Complement Activation; Complement C1 Inactivator Proteins - therapeutic use; Complement Inactivator Proteins - therapeutic use; Complement System Proteins - metabolism; Disease Models, Animal; Elapid Venoms - therapeutic use; Endothelia; Humans; Immunotherapy; Inflammation; Inflammation Mediators - immunology; Inflammation Mediators - metabolism; Ischemia; Lectins - immunology; Mannose-binding lectin; Mice; Mice, Knockout; Myocardial Reperfusion Injury - drug therapy; Myocardial Reperfusion Injury - etiology; Myocardial Reperfusion Injury - immunology; Oxidative Stress - immunology; Endothelia; Inflammation; Complement; Ischemia; Mannose-binding lectin; Immunotherapy
• ISSN: 0161-5890; 1872-9142
• DOI: 10.1016/S0161-5890(99)00116-9

It is clear that complement plays an important role in the inflammatory process following oxidative stress in cellular and animal models. Clinical trials underway with novel complement inhibitors will establish the potential therapeutic benefit of complement inhibition in human disease. For as much as we understand about the role of complement in disease states, many questions remain. How is complement activated on endothelial cells following oxidative stress? What is the ligand for MBL on endothelial cells following oxidative stress? Will inhibition of MBL provide tissue protection to the extent observed with other complement inhibitors such as sCR1 or anti-C5 mAbs? These questions and more will undoubtedly be answered in the next millennium.