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The anti-inflammatory effects of platelet-derived microparticles in human plasmacytoid dendritic cells involve liver X receptor activation

Innate immune responses play a critical role in atherosclerosis progression. Beside the well-known implication of macrophages,1 plasmacytoid dendritic cells (PDC) emerge as cells present in atherosclerotic lesions that may participate in or regulate atherosclerosis.2 These cells can exert both pro- and anti-inflammatory functions.3 This is the case of other cellular messengers, namely microparticles (MP),4 also implicated in atherosclerosis.4 Depending on their cellular origin, MP could either activate or inhibit PDC inflammatory responses.5 However, signaling pathways involved in these PDC responses still have to be identified. As membrane-derived by-products, MP after internalization can be a source of intracellular cholesterol derivatives6 that trigger liver X receptors (LXR).7 LXR are nuclear receptors regulating innate immune responses,8 including cell-derived by-product internalization, such as apoptotic bodies9 that belong together with MP to extracellular vesicles. Here, implication of the LXR pathway in MP engulfment by PDC and the subsequent PDC inflammatory responses were investigated.