Lutz HU Stammler P Bianchi V Trüeb RM Hunziker T Burger R Jelezarova E Späth PJ 2004 Intravenously applied normal human immunoglobulin G (IgG) has anti-inflammatory effects in the treatment of autoimmune diseases. Systemic inflammation can originate from an overreacting amplification loop of the complement system. In blood, C3b2-containing complexes maintain complement amplification much better than the extremely short-lived C3b. Therefore, in patients with the complement-dependent autoimmune disease, dermatomyositis, we studied whether intravenously applied normal human IgG (IVIG) stimulated in vivo inactivation of these complexes. In the course of IVIG treatment, clinically effective in 6 of 8 patients, the concentration of C3b2-containing complexes dropped to 37% +/- 14% (n = 6) of the pretreatment level when having infused 0.5 g IgG/kg body weight, increased marginally and in parallel to factor Bb thereafter until full-dose IgG was infused. By day 14 following infusion of 2 g IgG/kg body weight the concentration of C3b2-containing complexes was 66% +/- 19%. The plasma concentration of C3 remained constant in myopathic or increased by 15% to 20% in amyopathic patients. In contrast to this, IVIG infusion was associated with consumption of up to 40% of plasma C4 at day 1 to 2 after completion of IVIG infusion. Thus, IVIG had an immediate and long-lasting attenuating effect on complement amplification in vivo, despite the fact that it induced classical complement pathway activation. application/pdf https://sonar.ch/global/documents/162 eng info:eu-repo/semantics/altIdentifier/doi/10.1182/blood-2003-05-1530 info:eu-repo/semantics/altIdentifier/pmid/14512320 info:eu-repo/semantics/openAccess Blood. - 2004 Autoimmune Diseases Complement C3 Complement C3-C5 Convertases Complement C3b Complement C4 Complement System Proteins Dermatomyositis Gene Amplification Humans Immunoglobulin G Immunoglobulins, Intravenous Treatment Outcome Intravenously applied IgG stimulates complement attenuation in a complement-dependent autoimmune disease at the amplifying C3 convertase level. http://purl.org/coar/resource_type/c_6501