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  Indian J Med Microbiol
 

Figure 1: Plasma low-density lipoproteins (LDL) enter through the arterial wall. LDLs accumulate in mononuclear phagocytes through scavenger receptors. Later, lipid-laden macrophage foam cells die. Death of lipid-rich macrophage foam cells resulted in the accumulation of extracellular cholesteryl ester and cholesterol monohydrate crystals in the lipid-enriched necrotic cores of the plaque. Cholesterol crystals can trigger the activation of the inflammasome that generates biologically active version of the proinflammatory cytokines Interleukin-1 β (IL-1) and IL-18

Figure 1: Plasma low-density lipoproteins (LDL) enter through the arterial wall. LDLs accumulate in mononuclear phagocytes through scavenger receptors. Later, lipid-laden macrophage foam cells die. Death of lipid-rich macrophage foam cells resulted in the accumulation of extracellular cholesteryl ester and cholesterol monohydrate crystals in the lipid-enriched necrotic cores of the plaque. Cholesterol crystals can trigger the activation of the inflammasome that generates biologically active version of the proinflammatory cytokines Interleukin-1 β (IL-1) and IL-18