The influence of pro-inflammatory cytokines on lipid metabolism and the pro-atherogenic potential of immune cells in RA (IMAGE)
Caption
Pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) are produced in large quantities locally in the joints and subsequently enter the bloodstream. TNF-α and IL-6 may promote LDL metabolism by increasing the expression of LDLR and SR-B1 on the surface of liver cells. Moreover, TNF-α and IL-1β can reduce the formation of pro-ApoA1 particles in the liver by suppressing HDL production. Presentation of antigenic peptides from ApoB by antigen-presenting cells (APCs) promotes the formation of effector T cells from naïve (CD4+) T helper cells. APCs oxidize LDL-C particles, process, and present peptides from ApoB on major histocompatibility complex molecules. The specific T cell receptor is responsible for recognizing antigen fragments in the form of peptides bound to major histocompatibility complex molecules. Under the influence of co-stimulatory signals and cytokines secreted by APCs, T cells express transcription factors that promote differentiation into distinct Th types, which produce specific cytokines that can act both atheroprotectively and proatherogenic. anti-apoA1, antibodies against apolipoprotein A1; anti-HDL-Ab, anti-HDL antibodies; APCs, antigen-presenting cells; CRP, C-reactive protein; HDL, high-density lipoproteins; ICAM-1, intercellular adhesion molecule 1; IL, interleukin; LDL-C, low-density lipoprotein cholesterol; LDLR, low density lipoprotein receptor; LPC, lysophosphatidylcholine; MHC, major histocompatibility complex; ox-LDL, oxidized low-density lipoproteins; RA, rheumatoid arthritis; SR, scavenger receptor; TCR, T-cell receptor; Th, T helper; TNF, tumor necrosis factor; VCAM-1, vascular cellular adhesion molecule-1.
Credit
Elena V. Gerasimova, Tatiana V. Popkova
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License
CC BY-NC