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Neuroinflammation and brain lipid imbalances are observed in Alzheimer’s disease (AD). Tumor necrosis factor-α (TNFα) and the liver X receptor (<i>LXR</i>) signaling pathways are involved in both processes. However, limited information is currently available regarding their relationships in human brain pericytes (HBP) of the neurovascular unit. In cultivated HBP, TNFα activates the <i>LXR</i> pathway and increases the expression of one of its target genes, the transporter ATP-binding cassette family A member 1 (<i>ABCA1</i>), while <i>ABCG1</i> is not expressed. Apolipoprotein E (<i>APOE</i>) synthesis and release are diminished. The cholesterol efflux is promoted, but is not inhibited, when <i>ABCA1</i> or <i>LXR</i> are blocked. Moreover, as for TNFα, direct <i>LXR</i> activation by the agonist (T0901317) increases <i>ABCA1</i> expression and the associated cholesterol efflux. However, this process is abolished when <i>LXR</i>/<i>ABCA1</i> are both inhibited. Neither the other ABC transporters nor the SR-BI are involved in this TNFα-mediated lipid efflux regulation. We also report that inflammation increases <i>ABCB1</i> expression and function. In conclusion, our data suggest that inflammation increases HBP protection against xenobiotics and triggers an <i>LXR</i>/<i>ABCA1</i> independent cholesterol release. Understanding the molecular mechanisms regulating this efflux at the level of the neurovascular unit remains fundamental to the characterization of links between neuroinflammation, cholesterol and HBP function in neurodegenerative disorders.