TLR Signaling: An Emerging Bridge from Innate Immunity to Atherogenesis

Chronic inflammation and disordered lipid metabolism represent hallmarks of atherosclerosis. Considerable evidence suggests that innate immune defense mechanisms might interact with proinflammatory pathways and contribute to development of arterial plaques. The preponderance of such evidence has bee...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2004-11, Vol.173 (10), p.5901-5907
Main Authors: Michelsen, Kathrin S, Doherty, Terence M, Shah, Prediman K, Arditi, Moshe
Format: Article
Language:English
Subjects:
Animals
Arteriosclerosis - immunology
Arteriosclerosis - metabolism
Arteriosclerosis - microbiology
Arteriosclerosis - prevention & control
Humans
Immunity, Innate - genetics
Membrane Glycoproteins - genetics
Membrane Glycoproteins - physiology
Receptors, Cell Surface - genetics
Receptors, Cell Surface - physiology
Signal Transduction - genetics
Signal Transduction - immunology
Toll-Like Receptor 4
Toll-Like Receptors
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Summary:Chronic inflammation and disordered lipid metabolism represent hallmarks of atherosclerosis. Considerable evidence suggests that innate immune defense mechanisms might interact with proinflammatory pathways and contribute to development of arterial plaques. The preponderance of such evidence has been indirect clinical and epidemiologic studies, with some support from experimental animal models of atherosclerosis. However, recent data now directly implicate signaling by TLR4 in the pathogenesis of atherosclerosis, establishing a key link between atherosclerosis and defense against both foreign pathogens and endogenously generated inflammatory ligands. In this study, we briefly review these and closely related studies, highlighting areas that should provide fertile ground for future studies aimed at a more comprehensive understanding of the interplay between innate immune defense mechanisms, atherosclerosis, and related vascular disorders.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.173.10.5901