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Myelin-containing macrophages and microglia are the most abundant immune cells in active multiple sclerosis (MS) lesions. Our recent transcriptomic analysis demonstrated that collectin placenta 1 (CL-P1) is one of the most potently induced genes in macrophages after uptake of myelin. CL-P1 is a type II transmembrane protein with both a collagen-like and carbohydrate recognition domain, which plays a key role in host defense. In this study we sought to determine the dynamics of CL-P1 expression on myelin-containing phagocytes and define the role that it plays in MS lesion development. We show that myelin uptake increases the cell surface expression of CL-P1 by mouse and human macrophages, but not by primary mouse microglia in vitro. In active demyelinating MS lesions, CL-P1 immunoreactivity was localized to perivascular and parenchymal myelin-laden phagocytes. Finally, we demonstrate that CL-P1 is involved in myelin internalization as knockdown of CL-P1 markedly reduced myelin uptake. Collectively, our data indicate that CL-P1 is a novel receptor involved in myelin uptake by phagocytes and likely plays a role in MS lesion development.

Genome wide association studies have been linked the CDKN2A/B locus to an increased risk for atherosclerosis, type 2 diabetes and aneurysm development. These conditions all are linked to perivascular adipose tissue (pAT) accumulation, which has an inflammatory phenotype.

During obesity, inflammatory ‘M1’ macrophages infiltrate adipose tissue (AT). These ‘M1’ AT macrophages (ATMs) express the dendritic cell marker CD11c. Dendritic cells are immune regulators that promote insulin resistance. However, it is unclear whether and how CD11c+ ATMs differ from dendritic cells and if they are activated by obesity.

Heart attack and stroke, major causes of death in diabetes, are caused by plaque rupture, in which metabolic characteristics of the plaque are major determinants.