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Activation of the innate immune system in atherosclerotic disease

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Author: Oude Nijhuis, M.M. · Keulen, J.K. van · Pasterkamp, G. · Quax, P.H. · Kleijn, D.P.V. de
Institution: TNO Kwaliteit van Leven
Source:Current Pharmaceutical Design, 10, 13, 983-994
Identifier: 239930
doi: doi:10.2174/138161207780487593
Keywords: Biomedical Research · Atherogenesis · Infection · Inflammation · Innate immunity · Toll-like receptors · antibiotic agent · azithromycin · e 5331 · e 5531 · e 5564 · eritoran · ligand · lipid A derivative · lipopolysaccharide antagonist · low density lipoprotein · malonaldehyde · oxidized low density lipoprotein · placebo · receptor blocking agent · toll like receptor · vaccine · antigen recognition · atherogenesis · atherosclerosis · clinical trial · disease course · drug megadose · drug targeting · genetic polymorphism · human · innate immunity · knockout mouse · low drug dose · nonhuman · priority journal · review · signal transduction · vaccination · Animals · Atherosclerosis · Communicable Diseases · Humans · Immunity, Natural · Immunotherapy · Inflammation · Ligands · Lipopolysaccharides · Lipoproteins · Peptidoglycan · Signal Transduction · Toll-Like Receptors · Vaccines


Innate immunity is the first line of defence against invading micro-organisms. The family of Toll-like receptors (TLRs) recognizes pathogen-associated molecular patterns (PAMPs) that are carried by the invading micro-organisms. Infectious pathogens have been implicated to play an important role in atherosclerosis. Nowadays, evidence is accumulating that TLRs play an important role in the initiation and progression of atherosclerosis too. A lot is known about the exogenous ligands that are able to activate the TLRs, but it is also known that endogenous ligands have the capacity to activate TLRs when exogenous ligands are absent. Studies on knockout mice, epidemiological studies and even human polymorphism studies confirmed the important role of TLRs in development and progression of atherosclerotic disease. Studies with antagonists against TLR ligands and vaccination studies demonstrated that TLR signaling might be a potential target for intervention in the initiation and progression of atherosclerosis. © 2007 Bentham Science Publishers Ltd.