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The contact/kinin and complement systems in vasculitis.

Karpman, Diana LU and Kahn, Robin LU (2009) In APMIS Acta Pathologica, Microbiologica et Immunologica Scandinavica. Supplementum 117. p.48-54
Abstract
Vasculitides are a group of conditions with marked inflammation in and around vessel walls and vascular leakage. These conditions may involve the presence of auto-antibodies such as ANCA or may be mediated by other autoimmune or pathogenic mechanisms. Regardless of the primary trigger, vasculitides entail activation of the complement system as well as the contact/kinin system. In vivo and in vitro data support the involvement of these systems showing activation of the alternative, classical and lectin complement pathways as well as release of bradykinin at sites of vascular inflammation. This short review will summarize some of the data regarding the participation of these systems and the interplay between the complement and kinin systems... (More)
Vasculitides are a group of conditions with marked inflammation in and around vessel walls and vascular leakage. These conditions may involve the presence of auto-antibodies such as ANCA or may be mediated by other autoimmune or pathogenic mechanisms. Regardless of the primary trigger, vasculitides entail activation of the complement system as well as the contact/kinin system. In vivo and in vitro data support the involvement of these systems showing activation of the alternative, classical and lectin complement pathways as well as release of bradykinin at sites of vascular inflammation. This short review will summarize some of the data regarding the participation of these systems and the interplay between the complement and kinin systems as well as their interaction with the endothelium and neutrophils. Although these systems do not play a primary role in induction of vasculitis, the peptides released contribute to inflammation and vascular leakage and may thus be identified as potential therapeutic targets. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
APMIS Acta Pathologica, Microbiologica et Immunologica Scandinavica. Supplementum
volume
117
pages
48 - 54
publisher
Wiley-Blackwell
external identifiers
  • WOS:000268183700009
  • PMID:19515140
  • Scopus:66949161955
ISSN
0903-465X
DOI
10.1111/j.1600-0463.2009.02477.x
language
English
LU publication?
yes
id
ac0e944b-ff9c-4bbd-a517-ff594727f759 (old id 1452722)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19515140?dopt=Abstract
date added to LUP
2009-08-05 10:19:56
date last changed
2017-01-01 07:45:29
@article{ac0e944b-ff9c-4bbd-a517-ff594727f759,
  abstract     = {Vasculitides are a group of conditions with marked inflammation in and around vessel walls and vascular leakage. These conditions may involve the presence of auto-antibodies such as ANCA or may be mediated by other autoimmune or pathogenic mechanisms. Regardless of the primary trigger, vasculitides entail activation of the complement system as well as the contact/kinin system. In vivo and in vitro data support the involvement of these systems showing activation of the alternative, classical and lectin complement pathways as well as release of bradykinin at sites of vascular inflammation. This short review will summarize some of the data regarding the participation of these systems and the interplay between the complement and kinin systems as well as their interaction with the endothelium and neutrophils. Although these systems do not play a primary role in induction of vasculitis, the peptides released contribute to inflammation and vascular leakage and may thus be identified as potential therapeutic targets.},
  author       = {Karpman, Diana and Kahn, Robin},
  issn         = {0903-465X},
  language     = {eng},
  pages        = {48--54},
  publisher    = {Wiley-Blackwell},
  series       = {APMIS Acta Pathologica, Microbiologica et Immunologica Scandinavica. Supplementum},
  title        = {The contact/kinin and complement systems in vasculitis.},
  url          = {http://dx.doi.org/10.1111/j.1600-0463.2009.02477.x},
  volume       = {117},
  year         = {2009},
}