Complement activation and inhibition: a delicate balance
Sjoberg, A. P. ; Trouw, L. A. and Blom, Anna LU
(2009)
In Trends in Immunology
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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1401663
- author
- Sjoberg, A. P.
; Trouw, L. A.
and Blom, Anna
LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Trends in Immunology
- 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
- 2016-04-01 11:47:57
- date last changed
- 2022-03-05 06:35:54
@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 Immunology}},
title = {{Complement activation and inhibition: a delicate balance}},
url = {{http://dx.doi.org/10.1016/j.it.2008.11.003}},
doi = {{10.1016/j.it.2008.11.003}},
volume = {{30}},
year = {{2009}},
}