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Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions.

Karpman, Diana LU ; Ståhl, Anne-lie LU ; Arvidsson, Ida LU ; Johansson, Karl LU ; Loos, Sebastian LU ; Tati, Ramesh LU ; Békassy, Zivile LU ; Kristoffersson, Ann-Charlotte LU ; Mossberg, Maria LU and Kahn, Robin LU (2015) 1st International Conference on Immune Response to Biosurfaces In Advances in Experimental Medicine and Biology 865. p.19-42
Abstract
The complement system is activated in the vasculature during thrombotic and inflammatory conditions. Activation may be associated with chronic inflammation on the endothelial surface leading to complement deposition. Complement mutations allow uninhibited complement activation to occur on platelets, neutrophils, monocytes, and aggregates thereof, as well as on red blood cells and endothelial cells. Furthermore, complement activation on the cells leads to the shedding of cell derived-microvesicles that may express complement and tissue factor thus promoting inflammation and thrombosis. Complement deposition on red blood cells triggers hemolysis and the release of red blood cell-derived microvesicles that are prothrombotic. Microvesicles are... (More)
The complement system is activated in the vasculature during thrombotic and inflammatory conditions. Activation may be associated with chronic inflammation on the endothelial surface leading to complement deposition. Complement mutations allow uninhibited complement activation to occur on platelets, neutrophils, monocytes, and aggregates thereof, as well as on red blood cells and endothelial cells. Furthermore, complement activation on the cells leads to the shedding of cell derived-microvesicles that may express complement and tissue factor thus promoting inflammation and thrombosis. Complement deposition on red blood cells triggers hemolysis and the release of red blood cell-derived microvesicles that are prothrombotic. Microvesicles are small membrane vesicles ranging from 0.1 to 1 μm, shed by cells during activation, injury and/or apoptosis that express components of the parent cell. Microvesicles are released during inflammatory and vascular conditions. The repertoire of inflammatory markers on endothelial cell-derived microvesicles shed during inflammation is large and includes complement. These circulating microvesicles may reflect the ongoing inflammatory process but may also contribute to its propagation. This overview will describe complement activation on blood and endothelial cells and the release of microvesicles from these cells during hemolytic uremic syndrome, thrombotic thrombocytopenic purpura and vasculitis, clinical conditions associated with enhanced thrombosis and inflammation. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
in
Advances in Experimental Medicine and Biology
editor
Lambris, J.D.; Ekdahl, K.N.; Ricklin, D.; Nilsson, B.; ; ; and
volume
865
pages
19 - 42
publisher
Springer
conference name
1st International Conference on Immune Response to Biosurfaces
external identifiers
  • pmid:26306441
  • wos:000361838300003
  • scopus:84940388442
ISSN
0065-2598
ISBN
978-3-319-18602-3
DOI
10.1007/978-3-319-18603-0_2
language
English
LU publication?
yes
id
b6f34d62-c92e-4145-b2e8-964711c17ee6 (old id 7834631)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26306441?dopt=Abstract
date added to LUP
2015-09-07 20:37:44
date last changed
2017-09-17 06:03:35
@inproceedings{b6f34d62-c92e-4145-b2e8-964711c17ee6,
  abstract     = {The complement system is activated in the vasculature during thrombotic and inflammatory conditions. Activation may be associated with chronic inflammation on the endothelial surface leading to complement deposition. Complement mutations allow uninhibited complement activation to occur on platelets, neutrophils, monocytes, and aggregates thereof, as well as on red blood cells and endothelial cells. Furthermore, complement activation on the cells leads to the shedding of cell derived-microvesicles that may express complement and tissue factor thus promoting inflammation and thrombosis. Complement deposition on red blood cells triggers hemolysis and the release of red blood cell-derived microvesicles that are prothrombotic. Microvesicles are small membrane vesicles ranging from 0.1 to 1 μm, shed by cells during activation, injury and/or apoptosis that express components of the parent cell. Microvesicles are released during inflammatory and vascular conditions. The repertoire of inflammatory markers on endothelial cell-derived microvesicles shed during inflammation is large and includes complement. These circulating microvesicles may reflect the ongoing inflammatory process but may also contribute to its propagation. This overview will describe complement activation on blood and endothelial cells and the release of microvesicles from these cells during hemolytic uremic syndrome, thrombotic thrombocytopenic purpura and vasculitis, clinical conditions associated with enhanced thrombosis and inflammation.},
  author       = {Karpman, Diana and Ståhl, Anne-lie and Arvidsson, Ida and Johansson, Karl and Loos, Sebastian and Tati, Ramesh and Békassy, Zivile and Kristoffersson, Ann-Charlotte and Mossberg, Maria and Kahn, Robin},
  booktitle    = {Advances in Experimental Medicine and Biology},
  editor       = {Lambris, J.D. and Ekdahl, K.N. and Ricklin, D. and Nilsson, B.},
  isbn         = {978-3-319-18602-3},
  issn         = {0065-2598},
  language     = {eng},
  pages        = {19--42},
  publisher    = {Springer},
  title        = {Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions.},
  url          = {http://dx.doi.org/10.1007/978-3-319-18603-0_2},
  volume       = {865},
  year         = {2015},
}