|
|
||||||||
The Journal of Immunology, Vol 141, Issue 9 3117-3122, Copyright © 1988 by American Association of Immunologists
ARTICLES |
S Bhakdi, W Fassbender, F Hugo, MP Carreno, C Berstecher, P Malasit and MD Kazatchkine
Institute of Medical Microbiology, University of Giessen, West Germany.
The efficiency of generation of fluid-phase SC5b-9 and membrane C5b- 9(m) complexes relative to cleavage of C3 and C5 was studied. Fluid- phase C activation was induced through addition of purified bacterial Ag to human serum. Sephadex beads were used as particulate activators of the alternative pathway. Rabbit or antibody-coated sheep or human E were used to study formation of cytolytic C5b-9(m) complexes. The molar ratios of C3a:C5a generated in the model systems were found to be in the range of 60 to 200:1 in the case of soluble immune complex activators, and 70 to 150:1 with particulate activators and cells. The efficiency of C5 cleavage relative to C3 cleavage increased on surfaces with the density of antibody and/or C3b-binding sites. With soluble immune complexes, the efficiency of subsequent SC5b-9 generation displayed wide variations dependent on Ag and donor with molar ratios of C5a:SC5b-9 ranging from 30:1 for teichoic acid and sometimes approaching 1:1 for streptolysin-O. In contrast, activation on particles or cells always led to C5a:C5b-9 (calculated as the sum of generated moles SC5b-9 and C5b-9(m] ratios approaching 1:1. Hence, there is an overall inefficiency of terminal sequence activation in the C cascade due first to a dissociation at the level of C5 convertase formation/C5-cleavage and second, to a frequent inefficiency of C5b- utilization in the fluid-phase. The results provide an explanation for the very low levels of SC5b-9 found in plasma of healthy individuals and in patients with C-consuming immune complex disease.
This article has been cited by other articles:
![]() |
E. A. Lidington, D. O. Haskard, and J. C. Mason Induction of decay-accelerating factor by thrombin through a protease-activated receptor 1 and protein kinase C-dependent pathway protects vascular endothelial cells from complement-mediated injury Blood, October 15, 2000; 96(8): 2784 - 2792. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. C. Mason, H. Yarwood, K. Sugars, B. P. Morgan, K. A. Davies, and D. O. Haskard Induction of Decay-Accelerating Factor by Cytokines or the Membrane-Attack Complex Protects Vascular Endothelial Cells Against Complement Deposition Blood, September 1, 1999; 94(5): 1673 - 1682. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Avirutnan, P. Malasit, B. Seliger, S. Bhakdi, and M. Husmann Dengue Virus Infection of Human Endothelial Cells Leads to Chemokine Production, Complement Activation, and Apoptosis J. Immunol., December 1, 1998; 161(11): 6338 - 6346. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Rawal and M. K. Pangburn C5 Convertase of the Alternative Pathway of Complement. KINETIC ANALYSIS OF THE FREE AND SURFACE-BOUND FORMS OF THE ENZYME J. Biol. Chem., July 3, 1998; 273(27): 16828 - 16835. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. C. Mason, E. A. Lidington, S. R. Ahmad, and D. O. Haskard bFGF and VEGF synergistically enhance endothelial cytoprotection via decay-accelerating factor induction Am J Physiol Cell Physiol, March 1, 2002; 282(3): C578 - C587. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |