Abstract

Toll-like receptors belong to the pattern recognition receptor (PRR) group, which plays a major role in maintaining a balance between the host immune system and the microbial invasion. They are key factors in the early, innate defense mechanisms of the immune system, which are manifested by the activation of classical and alternative inflammatory pathways. Excessive activity of these receptors has been shown to cause homeostasis disorders, so that the response of cells with these receptors must be strictly regulated to prevent any harmful effects of their abnormal activation. Thus, cellular responses mediated through TLR receptors have to be strictly regulated in order to prevent potentially harmful effects of their abnormal activation. There is an increasing evidence to suggest, that the Toll-like receptors can initiate and accelerate a development of atherosclerosis. Activation of these receptors leads to enhanced proinflammatory cytokine synthesis, promotes accumulation of foam cells in the aorta and migration of vascular smooth muscle cells from tunica to intima media. The major challenge for development of the TLR blocking drugs is to reduce inflammation without affecting the innate immunity of a body. Although preclinical studies confirm that they are promising therapeutic targets and potential biomarkers in the pathogenesis of atherosclerosis, however it is necessary to fully define their functions.

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