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Innate immune molecular connections between atherosclerosis and statins: can the clinical laboratory venture beyond C-reactive protein?

Abstract

Innate immunity was originally envisioned as a nonspecific host response to microbial pathogens. However, in the past few years, immunologists have discovered toll-like receptors (TLRs) and their role in recognizing pathogen-associated molecular patterns. TLRs and other components of innate immunity now help to explain the pathologic mechanisms underlying many common diseases, including atherosclerosis. At this time, C-reactive protein is the most useful biomarker for evaluating the inflammatory aspect of atherogenesis. Yet, operating beneath this commonly assayed biomarker are other components of the immune response. These inflammatory components of atherosclerosis and their genetic variations provide important insights. Today, novel antiatherogenic therapies are emerging, and at the same time a molecular groundwork is being laid for the genetic testing of statin efficacy. However, the adoption of clinical testing will need to wait until new therapeutic choices enter medical practice.

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