In contrast, the Mac1 and Mac2 subsets, which were more prevalent in the adipose tissue of imiquimod-treated obese mice, exhibited downregulated genes that are characteristic of the lipid-associated macrophage signature, accompanied by decreased chromatin accessibility around the genes responsible for lipid handling and inflammatory migration, suggesting a failure to maintain lipid homeostasis and regulate metabolic inflammation, potentially exacerbating obesity-associated inflammatory responses in psoriasis. This evidence concerns the gene LGALS3 and obesity due to melanocortin 4 receptor deficiency.