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Prepublished online as a Blood First Edition Paper on September 25, 2003; DOI 10.1182/blood-2003-05-1530. This Article Full Text (PDF) All Versions of this Article: 2003-05-1530v1 103/2/465    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lutz, H. U Articles by Spaeth, P. J Search for Related Content PubMed PubMed Citation Articles by Lutz, H. U Articles by Spaeth, P. J Social Bookmarking                   What's this? Submitted May 20, 2003 Accepted September 6, 2003 Intravenously applied IgG stimulates complement attenuation in a complement-dependent auto-immune disease at the amplifying C3 convertase level Hans U Lutz*, Pia Stammler, Valentina Bianchi, Ralph M Trueb, Thomas Hunziker, Reinhard Burger, Emiliana Jelezarova, and Peter J Spaeth Institute of Biochemistry, Dept. Biology, Swiss Federal Institute of Technology, Zurich, Switzerland Department of Dermatology, University Hospital, Zurich, Switzerland Department of Dermatology, University Hospital, Bern, Switzerland Robert Koch Institut, Berlin, Germany Department of Immunology, ZLB Bioplasma AG, Bern, Switzerland * Corresponding author; email: hlutz{at}bc.biol.ethz.ch. Intravenously applied, normal human IgG (IVIG) has anti-inflammatory effects in treatment of autoimmune diseases. Systemic inflammation can originate from an overreacting amplification loop of the complement system. Activators of complement amplification in blood are C3b2-containing complexes and less the extremely short-lived C3b. Therefore, we studied in patients with the complement-dependent autoimmune disease, dermatomyositis, whether IVIG stimulated in vivo inactivation of these complexes. In the course of IVIG treatment, clinically effective in 6 out 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 b.w., increased marginally and in parallel to factor Bb thereafter until full dose IgG was infused. By day 14 following infusion of 2g IgG/kg b.w. 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 1-2 after completion of IVIG infusion. Thus, IVIG had an immediate and long lasting attenuating effect on complement amplification in vivo, despite it induced classical complement pathway activation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. C. Dimayuga, F. H. Y. Cesena, K.-Y. Chyu, J. Yano, A. Amorn, M. C. Fishbein, P. K. Shah, and B. Cercek Natural antibodies and complement modulate intimal thickening after arterial injury Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2009; 297(5): R1593 - R1600. [Abstract] [Full Text] [PDF] S. C. Jordan and M. D. Pescovitz Presensitization: The Problem and Its Management Clin. J. Am. Soc. Nephrol., May 1, 2006; 1(3): 421 - 432. [Abstract] [Full Text] [PDF] G. B. Appel, H. T. Cook, G. Hageman, J. C. Jennette, M. Kashgarian, M. Kirschfink, J. D. Lambris, L. Lanning, H. U. Lutz, S. Meri, et al. Membranoproliferative Glomerulonephritis Type II (Dense Deposit Disease): An Update J. Am. Soc. Nephrol., May 1, 2005; 16(5): 1392 - 1403. [Abstract] [Full Text] [PDF]

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