Lipid-Immunity Cross-Talk

Atherosclerotic disease remains a leading cause of death, despite significant improvements in treatment and prevention of primary disease manifestations. The increasing incidence of obesity and diabetes mellitus type 2 will further accelerate the global morbidity attributable to atherosclerotic disease. Atherosclerosis is considered an autoimmune-like inflammatory disease that proceeds in the presence of enhanced plasma cholesterol levels.1 Research groups that attempt to disentangle the pathogenesis of atherosclerotic disease often focus on either the role of the local inflammatory response or that of lipid metabolism and lipoprotein profiles. Answers to some unresolved questions in this research area could be obtained from studies that explore the cross-talk between lipids and inflammatory responses. There is sufficient evidence supporting the view that better understanding of the interaction between dyslipidemia and the immune response may help to unravel the pathogenesis of atherosclerotic disease progression. For example, it has been shown that lipid loading induces a distinct, unique gene expression profile in macrophages within the atherosclerotic lesion.2 In line with the induction of a specific gene expression profile upon lipid loading, monocytes from apolipoprotein E–deficient mice …