The expression of CD11c has previously been shown to associate with proinflammatory macrophage phenotype in obesity.31 Loss of aortic CD11c gene expression in IRF5-deficient mice was associated with a reduction in the aortic expression of proinflammatory genes such as iNOS and tumor necrosis factor-α, and an increase in genes associated with alternatively activated macrophages such as interleukin 4and IRF4, indicating that IRF5 is responsible for a shift toward a proinflammatory myeloid cell programming in atherosclerosis. This evidence concerns the gene NOS2 and atherosclerosis.