Nr1h3, also known as Liver-X-Receptor α (LXRα), is a key regulator in lipid metabolism. It controls macrophage polarization and the inflammatory response by regulating lipid metabolism, and is involved in numerous biological processes. Its activation can influence the expression of genes related to cholesterol efflux, such as ABCA1, playing a vital role in maintaining cholesterol homeostasis [6,7].

In diffuse large B-cell lymphoma (DLBCL), Nr1h3 is associated with the tumor microenvironment, and its high expression in M1-like pro-inflammatory macrophages predicts longer patient survival [1]. In non-segmental vitiligo, the SNP rs3758672 in Nr1h3 is associated with disease susceptibility and therapeutic effects, with the A allele increasing the risk and worsening treatment outcomes [2]. In multiple sclerosis, the p.Arg415Gln mutation in Nr1h3 disrupts its heterodimerization and transcriptional activation, and common variants like rs2279238 confer an increased risk of progressive MS [3,4]. In pulmonary tuberculosis patients, the mRNA expression of Nr1h3 is down-regulated [5].

In conclusion, Nr1h3 is crucial for lipid metabolism, macrophage regulation, and inflammation. Studies on Nr1h3, including those using genetic models, have revealed its significance in diseases such as lymphoma, vitiligo, multiple sclerosis, and tuberculosis, offering potential therapeutic targets for these conditions.