Neisseria meningitidis is an obligate human pathogen. When it interacts with the host, it can establish a commensal relationship or can, on a minority of occasions, invade and cause systemic disease. Protection against systemic disease, particularly for serogroup A and C infections, has been equated with the presence of bactericidal antibody directed against the capsular polysaccharide (CPS) (1). In serogroup B infections, the CPS resembles host-cell moieties, is non-immunogenic, and does not induce protection (2). Hence other components of the bacterial-cell envelope, such as outer-membrane proteins (OMPs), and cellular mechanisms of host defense, such as phagocytosis, have been implicated in immunity to serogroup B infections (3,4).