Abstract

### IgE Stimulates Human and Mouse Arterial Cell Apoptosis and Cytokine Expression and Promotes Atherogenesis in Apoe –/– Mice Wang et al J Clin Invest . 2011;121:3564–3577. A new report in the Journal of Clinical Investigation adds to the ever-increasing evidence that immunological mechanisms play an important role in atherogenesis. These new observations suggest involvement of IgE and its FcϵR1α receptor in the promotion of atherosclerosis, and specifically in plaque instability and clinical events. Evidence continues to accumulate supporting an important role for immunological mechanisms in all phases of atherosclerosis.1–3 Previous studies have supported an important modulating role for disease-specific IgG and IgM and for Fcγ receptors in modulating atherogenesis.4–9 In a recent report, Wang et al contribute to this growing body of literature by presenting novel observations supporting a proatherogenic role for IgE and its high-affinity receptor FcϵR1α.10 The authors compared the extent of atherosclerosis in wild-type apoE –/– mice fed a Western diet with apoE –/– / FcϵR1 α–/– mice and observed a profound reduction in lesion formation. Although nearly all the cell types known to be involved in atherogenesis express FcϵR1α receptors in vivo, the authors focused primarily on the potential role of this receptor in macrophage biology and demonstrated that IgE mediates a variety of proinflammatory effects in macrophages, such as release of interleukin-6 and monocyte chemoattractant protein-1, as well as proteases …

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