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A complex atherosclerotic phenotype of Mif gene-deficient mice in an atherogenic ApoE-/- background uncovers a novel connection between MIF and B cells

      Objectives: Macrophage migration inhibitory factor (MIF) is a chemokine-like inflammatory mediator that plays an important role in inflammatory diseases. MIF has been found to promote atherogenesis in several models. However, recent data suggest that MIF has a complex role in cardiovascular disease (CVD) including cardioprotective effects in models of myocardial ischemia/reperfusion injury. Here, we studied the impact of Mif gene deletion in the ApoE-/- background .
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