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. 2019 Dec 4;19(6):e41. doi: 10.4110/in.2019.19.e41

Figure 5. A schematic diagram illustrates the role of PCSK9 mediates atherosclerosis via immune cells.

Figure 5

This diagram displays the role of PCSK9 in atherosclerosis and immune response mediated via IL-17 cells and other immune cells including Th1, Treg and Tfh cells. Under normal lipidemic condition with low PCSK9 levels, the hepatocytes produce and secrete normal LDLs, these LDLs do not influence the development of atherosclerosis. Under hyperlipidemia condition with increased PCSK9 levels, the hepatocytes produce increased amounts of modified LDLs, which are cholesterol ester and phospholipid enriched. These modified LDLs contribute to the development of atherosclerosis by possibly altering T cells programing shifted towards IL-17 producing T cells to increase IL-17 production or via induce cytokines production to modulating immune cells including Th1, Treg or Tfh T cells to influence IL-17 production. Increased IL-17 contributes to the development of atherosclerosis.