Key result
Toll-like receptor activation drives atherogenesis by triggering vascular inflammation, lipid uptake, and foam cell formation.
Inflammation drives atherosclerosis. Both immune and resident vascular cell types are involved in the development of atherosclerotic lesions. The phenotype and function of these cells are key in determining the development of lesions. Toll-like receptors are the most characterised innate immune receptors and are responsible for the recognition of exogenous conserved motifs on pathogens, and, potentially, some endogenous molecules. Both endogenous and exogenous TLR agonists may be present in atherosclerotic plaques. Engagement of toll-like receptors on immune and resident vascular cells can affect atherogenesis as signalling downstream of these receptors can elicit proinflammatory cytokine release, lipid uptake, and foam cell formation and activate cells of the adaptive immune system. In this paper, we will describe the expression of TLRs on immune and resident vascular cells, highlight the TLR ligands that may act through TLRs on these cells, and discuss the consequences of TLR activation in atherosclerosis.
No takes yet. Share an insight, caveat, or question.
Cole et al. (2010) conducted a review in Atherosclerosis. Toll-like receptors was evaluated. Engagement of toll-like receptors on immune and resident vascular cells affects atherogenesis by eliciting proinflammatory cytokine release, lipid uptake, and foam cell formation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:
More from Mediators of Inflammation