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Complement system on the attack in autoimmunity
John P. Atkinson
Published in Volume 112, Issue 11
J Clin Invest. 2003; 112(11):1639–1641 doi:10.1172/JCI20309
This article Copyright © 2003, The American Society for Clinical Investigation
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Figure 1

C3b can be deposited on a target by immune complexes that commonly engage the classical pathway, by lectins such as mannose-binding protein that bind to sugars, or through the continuous low-grade turnover of the AP. The deposited C3b serves as a nidus for amplification of C3b deposition via the positive feedback loop. Control of this amplification process is critical to prevent undesirable injury to host cells. The presence of antibodies or lectins on a membrane at a site relatively lacking in membrane regulators is conducive to excessive complement activation on self tissue.

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