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Contribution of interactions between complement inhibitor C4b-binding protein and pathogens to their ability to establish infection with particular emphasis on Neisseria gonorrhoeae.

Blom, Anna LU and Ram, Sanjay (2008) In Vaccine 26 Suppl 8. p.49-55
Abstract
Complement activation and resulting opsonisation with C3b form key arms of the innate immune defense against infections. However, a wide variety of pathogens subvert complement attack by binding host complement inhibitors, which results in diminished opsonophagocytosis and killing of bacteria by lysis. Human C4b-binding protein (C4BP) binds Neisseria gonorrhoeae and Streptococcus pyogenes, both uniquely human pathogens. This binding specificity is circumvented by other bacterial species, which bind C4BP from numerous mammalian hosts that they infect. Binding of C4BP to Neisseria is mediated by outer membrane porin proteins and appears to be one of the main factors mediating serum resistance. Targeting C4BP binding sites on bacterial... (More)
Complement activation and resulting opsonisation with C3b form key arms of the innate immune defense against infections. However, a wide variety of pathogens subvert complement attack by binding host complement inhibitors, which results in diminished opsonophagocytosis and killing of bacteria by lysis. Human C4b-binding protein (C4BP) binds Neisseria gonorrhoeae and Streptococcus pyogenes, both uniquely human pathogens. This binding specificity is circumvented by other bacterial species, which bind C4BP from numerous mammalian hosts that they infect. Binding of C4BP to Neisseria is mediated by outer membrane porin proteins and appears to be one of the main factors mediating serum resistance. Targeting C4BP binding sites on bacterial surfaces with vaccine-induced antibodies may block binding of C4BP and 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
keywords
Serum resistance, Complement, Porin, Neisseria gonorrhoeae, C4b-binding protein
in
Vaccine
volume
26 Suppl 8
pages
49 - 55
publisher
Elsevier
external identifiers
  • pmid:19388165
  • wos:000263005500010
  • scopus:57749204785
ISSN
1873-2518
DOI
10.1016/j.vaccine.2008.11.049
language
English
LU publication?
yes
id
35c94321-91c1-4d9e-8bba-f0aafe5daaf5 (old id 1391915)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19388165?dopt=Abstract
date added to LUP
2009-05-05 15:41:07
date last changed
2017-08-20 04:36:34
@article{35c94321-91c1-4d9e-8bba-f0aafe5daaf5,
  abstract     = {Complement activation and resulting opsonisation with C3b form key arms of the innate immune defense against infections. However, a wide variety of pathogens subvert complement attack by binding host complement inhibitors, which results in diminished opsonophagocytosis and killing of bacteria by lysis. Human C4b-binding protein (C4BP) binds Neisseria gonorrhoeae and Streptococcus pyogenes, both uniquely human pathogens. This binding specificity is circumvented by other bacterial species, which bind C4BP from numerous mammalian hosts that they infect. Binding of C4BP to Neisseria is mediated by outer membrane porin proteins and appears to be one of the main factors mediating serum resistance. Targeting C4BP binding sites on bacterial surfaces with vaccine-induced antibodies may block binding of C4BP and enhance a common vaccine design strategy that depends on the generation of complement-dependent bactericidal and opsonophagocytic antibody activities.},
  author       = {Blom, Anna and Ram, Sanjay},
  issn         = {1873-2518},
  keyword      = {Serum resistance,Complement,Porin,Neisseria gonorrhoeae,C4b-binding protein},
  language     = {eng},
  pages        = {49--55},
  publisher    = {Elsevier},
  series       = {Vaccine},
  title        = {Contribution of interactions between complement inhibitor C4b-binding protein and pathogens to their ability to establish infection with particular emphasis on Neisseria gonorrhoeae.},
  url          = {http://dx.doi.org/10.1016/j.vaccine.2008.11.049},
  volume       = {26 Suppl 8},
  year         = {2008},
}