Complement protein expression and activation control central aspects of the normal B cell response. Imbalances in these processes invariably lead to autoimmune disease. Complement activation causes tissue damage in a number of ways and may by itself lead to autoimmune disease. Although the use of complement activation inhibitors in the treatment of complement-mediated tissue injury and disease is largely in pre-clinical trials, the expectations that they will be of significant clinical value are high. This volume contains a series of review articles that address the role of complement in the pathogenesis of autoimmune disease and the ensuing tissue damage. Topics include structural and functional aspects of the CD19/CD21/CD81 complex, role of the complement system in the expression of systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome. Also featured is the role of complement activation in ischemia/reperfusion and autoimmune disease injury. Finally, in-depth reviews about complement activation in the development of glomerulonephritis in autoimmune disease and the function of membrane-bound complement regulatory proteins in autoimmunity are presented. Students as well as basic and clinical researchers in immunology who wish to understand the role of complement in the pathogenesis of autoimmune disease will value this comprehensive and up-to-date publication.