Complement activation byN meningitidis. Lepirudin-anticoagulated human whole blood was incubated with 1 × 10⁸ heat-inactivated N meningitidis H44/76 for 1 hour at 37°C in the presence or absence of the following complement-inhibiting mAbs: anti-C2 (25 μg/mL), anti-MBL (100 μg/mL), and anti-factor D (25 μg/mL). C1rs-C1inh complexes (classical pathway; panel A), C4bc (classical and lectin pathways; panel B), and C3bBbP (alternative pathway; panel C) were used as markers of initial pathway activation, and fluid-phase terminal complement complex (TCC) was measured as an indicator of total complement activation (D). Minor spontaneous formation of all complement-activation products occurred in unstimulated blood (hatched columns). Meningococci (1 × 10⁸) induced a minor increase of C1rs-C1inh complex formation but significant C4bc, C3bBbP, and TCC formation (second columns). Anti-C2 had no statistically significant effect on any of the activation products, whereas anti-MBL completely inhibited C4bc formation, and anti-factor D completely inhibited alternative pathway activation. The increase in TCC was completely abolished by anti-factor D and was markedly reduced by anti-MBL. Median ± IQRs of 4 separately performed experiments are presented. ^*P < .05 compared with N meningitidis-stimulated sample (second columns).