Atherosclerosis is driven by inflammation with an involvement of innate and
adaptive immune responses. Toll-like receptors, the well-defined pattern recognition receptors
of the immune system, play a central role in macrophage activation. Toll-like receptors
recognize pathogen-associated molecular patterns expressed by a wide range of infectious
agents and provide a strong link between local innate and adaptive immunity. Activation of these receptors
triggers an intracellular signaling cascade mediated through myeloid differentiation factor 88 or
toll/interleukin-1 receptor-domain-containing adapter-inducing interferon-β, leading to the secretion of proand
anti-inflammatory cytokines. Engagement of Toll-like receptors with their ligands induces leukocyte recruitment
and enhances matrix metalloproteinase expression within atherosclerotic lesions. Recently certain
Toll-like receptors have shown a protective role in atherosclerosis. TLRs, therefore, represent an important
link between inflammation and atheroma, making them attractive targets for the treatment of atherosclerosis.
This review will briefly describe the general biological structure and potential roles of Toll-like receptors as
therapeutic targets for the treatment of atherosclerosis and highlight the potential challenges on Toll-like receptor-
based therapy in cardiovascular disease.
Keywords: Toll-like receptor, atherosclerosis, inflammation, plaque, cardiovascular disease, knock out mouse.
Rights & PermissionsPrintExport