Complement escape of human pathogenic bacteria by acquisition of complement regulators.
Pathogenic micro-organisms employ a broad range of strategies to survive in and to persistently infect the human host. Far from being completely understood by which highly sophisticated means invading pathogens overcome the host's destructive immune defence, there is a growing body of evidence on particular mechanisms which play a pivotal role for immune evasion. This review focuses on evasion of medically and scientifically important bacteria by acquisition of host derived fluid-phase complement regulatory proteins, in particular factor H, FHL-1, and C4b binding protein. Expression of microbial surface molecules binding to human complement regulators and thus fixing them in a functionally active state allows pathogens to inhibit and finely regulate complement activation directly on their surface. Further studies on the utilization of host complement regulatory proteins will likely have a marked impact on a more efficient and specific clinical treatment.
Kraiczy
Peter
P
Institute of Medical Microbiology, University Hospital of Frankfurt, Paul-Ehrlich-Str. 40, D-60596 Frankfurt, Germany. Kraiczy@em.uni-frankfurt.de
Würzner
Reinhard
R
D001419:Bacteria / Q000276:immunology* / Q000472:pathogenicity; D001424:Bacterial Infections / Q000276:immunology*; D001426:Bacterial Proteins / Q000276:immunology*; D003167:Complement Activation / Q000276:immunology*; D003180:Complement C3b Inactivator Proteins; D050716:Complement C4b-Binding Protein / Q000276:immunology*; D017242:Complement Factor H / Q000276:immunology*; D006801:Humans
D001426:Bacterial Proteins; C517621:CFHR1 protein, human; D003180:Complement C3b Inactivator Proteins; D050716:Complement C4b-Binding Protein; D017242:Complement Factor H