Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions.
(2015) 1st International Conference on Immune Response to Biosurfaces 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:
https://lup.lub.lu.se/record/7834631
- author
- 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
- organization
- publishing date
- 2015
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- host publication
- Advances in Experimental Medicine and Biology
- editor
- Lambris, J.D. ; Ekdahl, K.N. ; Ricklin, D. and Nilsson, B.
- volume
- 865
- pages
- 19 - 42
- publisher
- Springer
- conference name
- 1st International Conference on Immune Response to Biosurfaces
- conference dates
- 2014-08-27
- external identifiers
-
- pmid:26306441
- wos:000361838300003
- scopus:84940388442
- pmid:26306441
- 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
- 2016-04-01 13:26:36
- date last changed
- 2022-02-19 05:33:30
@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}}, doi = {{10.1007/978-3-319-18603-0_2}}, volume = {{865}}, year = {{2015}}, }