Protection from meningococcal disease involves both antimeningococcal immunoglobulins and complement. Activation of complement by antimeningococcal IgM or IgG promotes bacterial lysis via the membrane attack complex (C5–C9), while C3b [produced by alternative, mannose-binding lectin (MBL), or classic pathway activation] and antimeningococcal IgG₂ cooperate to produce effective opsonophagocytosis. A neutrophil defect in binding IgG₂ (the FcγRIIA R131 allele) has been associated with more severe meningococcal disease. CR1, complement receptor 1; LOS, lipooligosaccharide.