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Complement activation and inhibition: a delicate balance

Sjoberg, A. P.; Trouw, L. A. and Blom, Anna LU (2009) In Trends in Immunology2001-01-01+01:00 30(2). p.83-90
Abstract
Complement is part of the innate immune defence and not only recognizes microbes but also unwanted host molecules to enhance phagocytosis and clearance. This process of opsonisation must be tightly regulated to prevent immunopathology. Endogenous ligands such as dying cells, extracellular matrix proteins, pentraxins, amyloid deposits, prions and DNA, all bind the complement activator C1q, but also interact with complement inhibitors Cob-binding protein and factor H. This contrasts to the interaction between C1q and immune complexes, in which case no inhibitors bind, resulting in full complement activation. Disturbances to the complement regulation on endogenous ligands can lead to diseases such as age-related macular degeneration,... (More)
Complement is part of the innate immune defence and not only recognizes microbes but also unwanted host molecules to enhance phagocytosis and clearance. This process of opsonisation must be tightly regulated to prevent immunopathology. Endogenous ligands such as dying cells, extracellular matrix proteins, pentraxins, amyloid deposits, prions and DNA, all bind the complement activator C1q, but also interact with complement inhibitors Cob-binding protein and factor H. This contrasts to the interaction between C1q and immune complexes, in which case no inhibitors bind, resulting in full complement activation. Disturbances to the complement regulation on endogenous ligands can lead to diseases such as age-related macular degeneration, neurological and rheumatic disorders. A thorough understanding of these processes might be crucial to developing new therapeutic strategies. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Trends in Immunology2001-01-01+01:00
volume
30
issue
2
pages
83 - 90
publisher
Elsevier
external identifiers
  • wos:000264279300005
  • scopus:60349127531
ISSN
1471-4981
DOI
10.1016/j.it.2008.11.003
language
English
LU publication?
yes
id
d20c2cb7-dc9b-4942-af75-fe7a068cfade (old id 1401663)
date added to LUP
2009-06-15 09:42:30
date last changed
2017-12-10 03:42:27
@article{d20c2cb7-dc9b-4942-af75-fe7a068cfade,
  abstract     = {Complement is part of the innate immune defence and not only recognizes microbes but also unwanted host molecules to enhance phagocytosis and clearance. This process of opsonisation must be tightly regulated to prevent immunopathology. Endogenous ligands such as dying cells, extracellular matrix proteins, pentraxins, amyloid deposits, prions and DNA, all bind the complement activator C1q, but also interact with complement inhibitors Cob-binding protein and factor H. This contrasts to the interaction between C1q and immune complexes, in which case no inhibitors bind, resulting in full complement activation. Disturbances to the complement regulation on endogenous ligands can lead to diseases such as age-related macular degeneration, neurological and rheumatic disorders. A thorough understanding of these processes might be crucial to developing new therapeutic strategies.},
  author       = {Sjoberg, A. P. and Trouw, L. A. and Blom, Anna},
  issn         = {1471-4981},
  language     = {eng},
  number       = {2},
  pages        = {83--90},
  publisher    = {Elsevier},
  series       = {Trends in Immunology2001-01-01+01:00},
  title        = {Complement activation and inhibition: a delicate balance},
  url          = {http://dx.doi.org/10.1016/j.it.2008.11.003},
  volume       = {30},
  year         = {2009},
}