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Blood, 15 January 2004, Vol. 103, No. 2, pp. 465-472. Prepublished online as a Blood First Edition Paper on September 25, 2003; DOI 10.1182/blood-2003-05-1530. This Article Full Text 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 Citation Map 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 Späth, P. J. Search for Related Content PubMed PubMed Citation Articles by Lutz, H. U. Articles by Späth, P. J. Related Collections Transfusion Medicine Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS Intravenously applied IgG stimulates complement attenuation in a complement-dependent autoimmune disease at the amplifying C3 convertase level Hans U. Lutz, Pia Stammler, Valentina Bianchi, Ralph M. Trüeb, Thomas Hunziker, Reinhard Burger, Emiliana Jelezarova, and Peter J. Späth From the Institute of Biochemistry, Swiss Federal Institute of Technology, ETH-Hoenggerberg, Zurich, Switzerland; Department of Dermatology, University Hospital of Zurich, Zurich, Switzerland; Department of Dermatology, Inselspital, Berne, Switzerland; Robert Koch Institut, Berlin, Germany; and ZLB Bioplasma, Berne, Switzerland. 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. 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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