CD40LG and atherosclerosis: This is supported by the capacity of E06 to block OxLDL uptake by macrophages (87) and proinflammatory cytokine production by OxPL-stimulated macrophages (88) in vitro. While the expansion of OSE-specific IgM could be considered therapeutically in atherosclerosis, it is important to identify its right “therapeutic window.” This is essential as endogenous OSE-specific IgMs are present at high levels in both mice and humans (89) and increase over time in hypercholesterolemia (90).