Under lipotoxic conditions, Sdc4-deficient (sh-Sdc4) monocytes exhibited upregulated expression of CD206 (an M2 marker) and IL-10. When cocultured with sh-Sdc4 monocytes under palmitic acid stimulation, HepG2 cells accumulated fewer lipid droplets and producedlessTNF-α protein, along with increased IL-10 genes, compared to controls.