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Complement evasion strategies of pathogens-Acquisition of inhibitors and beyond.

Blom, Anna LU ; Hallström, Teresia LU and Riesbeck, Kristian LU (2009) In Molecular Immunology 46. p.2808-2817
Abstract
Activation of the complement system and resulting opsonisation with C3b are key events of the innate immune defense against infections. However, a wide variety of bacterial pathogens subvert complement attack by binding host complement inhibitors such as C4b-binding protein, factor H and vitronectin, which results in diminished opsonophagocytosis and killing of bacteria by lysis. Another widely used strategy is production of proteases, which can effectively degrade crucial complement components. Furthermore, bacterial pathogens such as Moraxella catarrhalis and Staphylococcus aureus capture and incapacitate the key complement component C3. The current review describes examples of these three strategies. Targeting binding sites for... (More)
Activation of the complement system and resulting opsonisation with C3b are key events of the innate immune defense against infections. However, a wide variety of bacterial pathogens subvert complement attack by binding host complement inhibitors such as C4b-binding protein, factor H and vitronectin, which results in diminished opsonophagocytosis and killing of bacteria by lysis. Another widely used strategy is production of proteases, which can effectively degrade crucial complement components. Furthermore, bacterial pathogens such as Moraxella catarrhalis and Staphylococcus aureus capture and incapacitate the key complement component C3. The current review describes examples of these three strategies. Targeting binding sites for complement inhibitors on bacterial surfaces and complement-degrading proteases with vaccine-induced antibodies may be used to enhance a common vaccine design strategy that depends on the generation of complement-dependent bactericidal and opsonophagocytic antibody activities. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Molecular Immunology
volume
46
pages
2808 - 2817
publisher
Pergamon
external identifiers
  • WOS:000269554500010
  • PMID:19477524
  • Scopus:68249086824
ISSN
1872-9142
DOI
10.1016/j.molimm.2009.04.025
language
English
LU publication?
yes
id
c69ad74c-3085-4c07-ba59-8d106e3b0162 (old id 1411918)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19477524?dopt=Abstract
date added to LUP
2009-06-03 14:39:26
date last changed
2016-11-27 04:28:19
@misc{c69ad74c-3085-4c07-ba59-8d106e3b0162,
  abstract     = {Activation of the complement system and resulting opsonisation with C3b are key events of the innate immune defense against infections. However, a wide variety of bacterial pathogens subvert complement attack by binding host complement inhibitors such as C4b-binding protein, factor H and vitronectin, which results in diminished opsonophagocytosis and killing of bacteria by lysis. Another widely used strategy is production of proteases, which can effectively degrade crucial complement components. Furthermore, bacterial pathogens such as Moraxella catarrhalis and Staphylococcus aureus capture and incapacitate the key complement component C3. The current review describes examples of these three strategies. Targeting binding sites for complement inhibitors on bacterial surfaces and complement-degrading proteases with vaccine-induced antibodies may be used to enhance a common vaccine design strategy that depends on the generation of complement-dependent bactericidal and opsonophagocytic antibody activities.},
  author       = {Blom, Anna and Hallström, Teresia and Riesbeck, Kristian},
  issn         = {1872-9142},
  language     = {eng},
  pages        = {2808--2817},
  publisher    = {ARRAY(0xb270a20)},
  series       = {Molecular Immunology},
  title        = {Complement evasion strategies of pathogens-Acquisition of inhibitors and beyond.},
  url          = {http://dx.doi.org/10.1016/j.molimm.2009.04.025},
  volume       = {46},
  year         = {2009},
}