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Science 13 July 1990:
Vol. 249. no. 4965, pp. 146 - 151
DOI: 10.1126/science.2371562
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Articles

Science, Vol 249, Issue 4965, 146-151
Copyright © 1990 by American Association for the Advancement of Science

articles

Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis

HF Weisman, T Bartow, MK Leppo, HC Marsh Jr, GR Carson, MF Concino, MP Boyle, KH Roux, ML Weisfeldt, and DT Fearon

Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.

The complement system is an important mediator of the acute inflammatory response, and an effective inhibitor would suppress tissue damage in many autoimmune and inflammatory diseases. Such an inhibitor might be found among the endogenous regulatory proteins of complement that block the enzymes that activate C3 and C5. Of these proteins, complement receptor type 1 (CR1; CD35) has the most inhibitory potential, but its restriction to a few cell types limits its function in vivo. This limitation was overcome by the recombinant, soluble human CR1, sCR1, which lacks the transmembrane and cytoplasmic domains. The sCR1 bivalently bound dimeric forms of its ligands, C3b and methylamine-treated C4 (C4-ma), and promoted their inactivation by factor I. In nanomolar concentrations, sCR1 blocked complement activation in human serum by the two pathways. The sCR1 had complement inhibitory and anti-inflammatory activities in a rat model of reperfusion injury of ischemic myocardium, reducing myocardial infarction size by 44 percent. These findings identify sCR1 as a potential agent for the suppression of complement-dependent tissue injury in autoimmune and inflammatory diseases.


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R. W. Brock, R. G. Nie, K. A. Harris, and R. F. Potter (2001)
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Expression of a Soluble Complement Inhibitor Protects Transgenic Mice from Antibody-Induced Acute Renal Failure.
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J. Immunol. 165, 2491-2499
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G. Peri, M. Introna, D. Corradi, G. Iacuitti, S. Signorini, F. Avanzini, F. Pizzetti, A. P. Maggioni, T. Moccetti, M. Metra, et al. (2000)
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J. Immunol. 165, 1059-1065
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A New Small Molecule C5a Receptor Antagonist Inhibits the Reverse-Passive Arthus Reaction and Endotoxic Shock in Rats.
A. J. Strachan, T. M. Woodruff, G. Haaima, D. P. Fairlie, and S. M. Taylor (2000)
J. Immunol. 164, 6560-6565
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Lipoteichoic Acid Induces Delayed Protection in the Rat Heart : A Comparison With Endotoxin.
K. Zacharowski, S. Frank, M. Otto, P. K. Chatterjee, S. Cuzzocrea, G. Hafner, J. Pfeilschifter, and C. Thiemermann (2000)
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Am. J. Respir. Crit. Care Med. 161, 1332-1339
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Complement Activation Products in the Urine from Proteinuric Patients.
Y. MORITA, H. IKEGUCHI, J. NAKAMURA, N. HOTTA, Y. YUZAWA, and S. MATSUO (2000)
J. Am. Soc. Nephrol. 11, 700-707
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Mesenteric dysfunction after cardiopulmonary bypass: role of complement C5a.
M. Tofukuji, G. L. Stahl, C. Metais, M. Tomita, A. Agah, C. Bianchi, M. P. Fink, and F. W. Sellke (2000)
Ann. Thorac. Surg. 69, 799-807
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C1-Esterase Inhibitor: An Anti-Inflammatory Agent and Its Potential Use in the Treatment of Diseases Other Than Hereditary Angioedema.
C. Caliezi, W. A. Wuillemin, S. Zeerleder, M. Redondo, B. Eisele, and C. E. Hack (2000)
Pharmacol. Rev. 52, 91-112
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Soluble Complement Receptor-1 Protects Heart, Lung, and Cardiac Myofilament Function From Cardiopulmonary Bypass Damage.
P. J. Chai, R. Nassar, A. E. Oakeley, D. M. Craig, G. Quick Jr, J. Jaggers, S. P. Sanders, R. M. Ungerleider, and P. A. W. Anderson (2000)
Circulation 101, 541-546
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A Soluble Recombinant Multimeric Anti-Rh(D) Single-Chain Fv/CR1 Molecule Restores the Immune Complex Binding Ability of CR1-Deficient Erythrocytes.
S. Oudin, M. T. Libyh, D. Goossens, X. Dervillez, F. Philbert, B. Reveil, F. Bougy, T. Tabary, P. Rouger, D. Klatzmann, et al. (2000)
J. Immunol. 164, 1505-1513
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