Abstract
Within just a few minutes the complement system (1) can label a foreign cell that has invaded the bloodstream with millions of copies of C3b. Destruction or clearance of the C3b-coated invader quickly follows. C3b is the activated cleavage product of C3, an abundant serum protein. Numerous diseases have been linked to collateral damage from this aggressive process (2). Recently, Ueda et al . (3) presented a striking example of a mouse model, based on a single amino-acid replacement, in which uncontrolled C3b deposition on host tissue led to renal failure, stroke and retinopathy.
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