Abstract
Background and Aims: Macrophage migration-inhibitory factor (MIF) is an inflammatory cytokine and atypical chemokine (ACK) that is upregulated in human atherosclerotic lesions and correlates with CAD. MIF is a pivotal driver of atherogenesis as evidenced in experimental atherosclerosis models employing Mif gene deletion or antibody neutralization approaches. Recent studies have examined the Mif gene deletion in an Apoe-/- background more closely and have revealed a link between MIF and B cell autoreactivity in atherosclerosis comprising i) vascular site-specific atheroprotection after 24 weeks of Western diet and ii) a reduction in peripheral B cells counts due to a maturation defect in the bone marrow (BM). Following up on these results, we aim to clarify the role of MIF and D-DT/MIF-2, a structural homolog of MIF, in atheroprotective B cell autoreactivity and B cell clustering with a focus on advanced lesions.
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