The identification of Toll-like receptors (TLRs) as key pattern recognition 

receptors of innate immunity has opened inquiries into previously unknown 

disease mechanisms. The ability of TLRs to detect a spectrum of pathogen-derived molecules defines their importance in innate immunity and provides a mechanistic link between infection and disease. Atherosclerosis is a chronic inflammatory disease where immune and metabolic factors interact to initiate and propagate arterial lesions. An understanding of TLRs in atherosclerosis could clarify the etiology of this complex process. 

Furthermore, the existence of host-derived endogenous TLR ligands implicates 

TLR involvement in disease mechanisms beyond innate immunity, such as a role 

in homeostatic mechanisms to resolve injury. Our recent data demonstrates an 

atherosclerotic role of TLR2 in hyperlipidemic mice. In situ immunofluorescence and laser scanning confocal microscopy of aortic segments reveal altered macrophage entry at sites of lesion predilection plays a role in the atheroprotective mechanism of TLR2 deficiency.