Figure 8.

Proposed genetic predisposition for dysregulated homeostasis/transport of lipid, lipoprotein, cholesterol, and fatty acid metabolism leading to lipid depositions in the salivary and lacrimal glands of C57BL/6.NOD-Aec1Aec2 mice and Sjögren syndrome patients. Accumulation of free cholesterols (FCs) inside the cells resulted from increased uptake of low- and high-density lipid receptors. In addition, impairment of ABCA1 membrane transporter leads to the accumulation of cholesteryl esters (CEs) metabolized by sterol O-acyltransferase-1 (SOAT-1) using FCs and free fatty acids (FFAs). ABCA1, ATP-binding cassette, subfamily A [ABC1] member 1; ACAT, acyl-coenzyme A: cholesterol acyltransferase; ApoE, apolipoprotein E; DC, dendritic cell; Fdft-1, farnesyl diphosphate farnesyl transferase-1; HDL, high-density lipid; LDL, low-density lipid; Lrpr, low-density lipid-related protein receptor; NCEH, neutral cholesterol esters hydrolase; Ox-LDL, oxidized low-density lipid; PPAR, peroxisome proliferator activated receptor; RANTES, regulated on activation normal T cell expressed and secreted; RXR, retinoid × receptor. Adapted from [48].