Open AccessActivation of Endothelial Toll-Like Receptor 3 Impairs Endothelial Function
Author(s) -
Sebastian Zimmer,
Martin Steinmetz,
Tobias Asdonk,
Inga Motz,
Christoph Coch,
Evelyn Hartmann,
Winfried Barchet,
Sven Waßmann,
Gunther Hartmann,
Georg Nickenig
Publication year - 2011
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.111.243246
Subject(s) - tlr3 , innate immune system , endothelial stem cell , endothelium , toll like receptor , biology , endothelial dysfunction , proinflammatory cytokine , vascular endothelial growth factor b , immunology , immune system , inflammation , microbiology and biotechnology , endocrinology , vascular endothelial growth factor a , biochemistry , vascular endothelial growth factor , in vitro , cancer research , vegf receptors
Endothelial dysfunction and atherosclerosis are chronic inflammatory diseases characterized by activation of the innate and acquired immune system. Specialized protein receptors of the innate immune system recognize products of microorganisms and endogenous ligands such as nucleic acids. Toll-like receptor 3 (TLR3), for example, detects long double-stranded RNA and is abundantly expressed in endothelial cells. Whether innate immunity contributes to atherogenic mechanisms in endothelial cells is poorly understood.
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