Model by which the classical and alternative complement pathways mediate SBA or OPA killing of meningococci. Blocking cleavage of C5 or C7 in the terminal complement pathway prevents formation of MAC, which is required for complement-mediated SBA. In the absence of MAC, anti-meningococcal antibodies may offer protection by eliciting antibody-Fc–mediated and/or C3b/iC3b complement receptor–mediated OPA. However, complement receptor–mediated phagocytic uptake as well as phagocytic cell chemotaxis is promoted by C5a, a split product of C5. Thus, blockage of release of C5a by eculizumab could abrogate this additional protective mechanism. See Figure 1 in the article by Konar and Granoff that begins on page 891.