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High-density lipoproteins (HDLs) are effective antioxidant, antiinflammatory, anti-thrombotic, and cardioprotective particles capable of exerting vasculoand cardioprotective effects. Yet the most relevant function of HDL is to promote reverse cholesterol transport, a mechanism by which HDL particles mediate the movement of cholesterol of peripheral cells to the liver for excretion in the bile. It has been well established that HDL interacts with lipid rafts found in the surface of lipid-loaded macrophage and depletes cholesterol from these microdomains either in an active way through the adenosine triphosphatebinding cassette (ABC) transporters ABCA1 and ABCG1 or a passive/ diffusional way (Figure 1). Through these mechanisms, HDL particles prevent foam cell formation, thereby protecting against atherosclerotic cardiovascular disease (CVD; Figure 1). During the last years, however, it has become evident that the ability of HDL particles to act as cholesterol acceptors modulating lipid raft structure also affects the innate and adaptive immunity. On the one hand, lipid rafts have been shown to function as platforms for the clustering and activation of toll-like receptors (TLRs), which are critically involved in the innate immune response by inducing cytokine and chemokine production, and on the other hand, lipid rafts contribute to the adaptive immune response, because they concentrate on major histocompatibility complex class II molecules in the cell surface of antigen-presenting cells. Low HDL-cholesterol levels represent an important cardiovascular risk factor, and, accordingly, it was assumed that increasing HDLcholesterol would exert beneficial effects in patients with symptomatic atherosclerotic heart disease. However, observations from genetic studies and the disappointing outcomes from multiple clinical trials aimed to raising HDL with pharmacological therapies have evidenced that HDL-cholesterol levels do not necessarily reflect protection against CVD. Moreover, human studies have evidenced that HDL function is better suited to predict CV events than HDL-cholesterol levels. For instance, a recent study in almost 3000 subjects free from CVD has linked impaired HDL-cholesterol efflux capacity with the prediction of atherosclerotic CV events. Autoimmune disease such as systemic lupus erythematosus (SLE), rheumatoid arthritis, and Crohn’s disease also feature low HDL-cholesterol levels suggesting a role for HDL particles in maintaining immune tolerance. As such, HDL particles have shown to suppress dendritic cell maturation and function thereby attenuating the adaptive immune response. Interestingly, in concurrence with the CVD setting, HDL function is found to be altered in several autoimmune-related disorders. So far, few studies in animal models have suggested a link between defects on cholesterol efflux in macrophages and lymphocytes with the Dr Gemma Vilahur is a Senior I3P Researcher at the Cardiovascular Science Institute (ICCC; Hospital Santa Creu and Sant Pau) in Barcelona, Spain, where she co-ordinates the Translational Research Department since her return from the USA in 2006. She is Principal Investigator and Co-Principal Investigator of multiple grants/projects (National and European) either funded by the Government and/or the Industry. Her research activities have been focused on cardiovascular research, especially devoting to elucidate the basic mechanisms underlying vascular and heart disease pathology (from atherosclerosis to ischaemic heart disease) and to discover and evaluate new potential therapeutic targets/ approaches. She has published multiple peer-reviewed articles and book chapters, is author of several patents, and has received many scientific awards.

High-density lipoprotein benefits beyond the cardiovascular system: a potential key role for modulating acquired immunity through cholesterol efflux