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Meningococcal infection remains a worldwide health problem, and understanding the mechanisms by which Neisseria meningitidis evades host innate and acquired immunity is crucial. The complement system is vital for protecting individuals against N. meningitidis. However, this pathogen has evolved several mechanisms to avoid killing by human complement. Bacterial structures such as polysaccharide capsule and those which mimic or bind host molecules function to prevent complement-mediated lysis and phagocytosis. This review provides an update on the recent findings on the diverse mechanisms by which N. meningitidis avoids complement-mediated killing, and how polymorphisms in genes encoding human complement proteins affect susceptibility to this important human pathogen.

Original publication

DOI

10.1016/j.tim.2007.03.005

Type

Journal article

Journal

Trends Microbiol

Publication Date

05/2007

Volume

15

Pages

233 - 240

Keywords

Bacterial Capsules, Complement Activation, Complement System Proteins, Genetic Predisposition to Disease, Humans, Immunity, Innate, Lipopolysaccharides, Meningococcal Infections, Models, Immunological, Neisseria meningitidis, Polymorphism, Genetic, Virulence