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

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Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions. / Karpman, Diana; Ståhl, Anne-lie; Arvidsson, Ida; Johansson, Karl; Loos, Sebastian; Tati, Ramesh; Békássy, Zivile; Kristoffersson, Ann-Charlotte; Mossberg, Maria; Kahn, Robin.

in: ADV EXP MED BIOL, Jahrgang 865, 2015, S. 19-42.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Transfer › Begutachtung

Harvard

Karpman, D, Ståhl, A, Arvidsson, I, Johansson, K, Loos, S, Tati, R, Békássy, Z, Kristoffersson, A-C, Mossberg, M & Kahn, R 2015, 'Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions', ADV EXP MED BIOL, Jg. 865, S. 19-42. https://doi.org/10.1007/978-3-319-18603-0_2

APA

Karpman, D., Ståhl, A., Arvidsson, I., Johansson, K., Loos, S., Tati, R., Békássy, Z., Kristoffersson, A-C., Mossberg, M., & Kahn, R. (2015). Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions. ADV EXP MED BIOL, 865, 19-42. https://doi.org/10.1007/978-3-319-18603-0_2

Vancouver

Karpman D, Ståhl A, Arvidsson I, Johansson K, Loos S, Tati R et al. Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions. ADV EXP MED BIOL. 2015;865:19-42. https://doi.org/10.1007/978-3-319-18603-0_2

Bibtex

@article{fc3fb0e30b794eaaadeea269cca69456,
title = "Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions",
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.",
keywords = "Blood Coagulation Factors, Blood Platelets, Cell-Derived Microparticles, Complement Activation, Complement System Proteins, Endothelial Cells, Erythrocytes, Hemolytic-Uremic Syndrome, Humans, Inflammation, Leukocytes, Purpura, Thrombotic Thrombocytopenic, Thrombosis, Vasculitis, Journal Article, Research Support, Non-U.S. Gov't, Review",
author = "Diana Karpman and Anne-lie St{\aa}hl and Ida Arvidsson and Karl Johansson and Sebastian Loos and Ramesh Tati and Zivile B{\'e}k{\'a}ssy and Ann-Charlotte Kristoffersson and Maria Mossberg and Robin Kahn",
year = "2015",
doi = "10.1007/978-3-319-18603-0_2",
language = "English",
volume = "865",
pages = "19--42",
journal = "ADV EXP MED BIOL",
issn = "0065-2598",
publisher = "Springer New York",

}

RIS

TY - JOUR

T1 - Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in Thrombotic and Inflammatory Conditions

AU - Karpman, Diana

AU - Ståhl, Anne-lie

AU - Arvidsson, Ida

AU - Johansson, Karl

AU - Loos, Sebastian

AU - Tati, Ramesh

AU - Békássy, Zivile

AU - Kristoffersson, Ann-Charlotte

AU - Mossberg, Maria

AU - Kahn, Robin

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

KW - Blood Coagulation Factors

KW - Blood Platelets

KW - Cell-Derived Microparticles

KW - Complement Activation

KW - Complement System Proteins

KW - Endothelial Cells

KW - Erythrocytes

KW - Hemolytic-Uremic Syndrome

KW - Humans

KW - Inflammation

KW - Leukocytes

KW - Purpura, Thrombotic Thrombocytopenic

KW - Thrombosis

KW - Vasculitis

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

KW - Review

U2 - 10.1007/978-3-319-18603-0_2

DO - 10.1007/978-3-319-18603-0_2

M3 - SCORING: Journal article

C2 - 26306441

VL - 865

SP - 19

EP - 42

JO - ADV EXP MED BIOL

JF - ADV EXP MED BIOL

SN - 0065-2598

ER -