Trim24, also known as TRIpartite motif-containing protein 24, is an E3 ligase and epigenetic regulator involved in multiple biological processes. It participates in pathways such as the STAT6-related macrophage polarization regulation, DNA double-strand break repair, and insulin-related mRNA stability regulation. It has significance in diseases including cancer, allergic rhinitis, and HIV-1 latency [1,3,4,5,6].

In macrophage polarization, Trim24-knockout (KO) in both mouse and human macrophages promotes M2 polarization potentially compromising antitumor immune responses, as Trim24 promotes Stat6 acetylation to suppress M2 polarization [1]. In nasopharyngeal carcinoma, depletion of TRIM24 inhibits M1 macrophage polarization, facilitating NPC cell growth and migration [2]. In DNA double-strand breaks, TRIM24-depleted human hepatocellular carcinoma cells are more sensitive to cancer therapy-induced apoptosis and show retarded tumor growth in a xenograft model, as TRIM24 is essential for MRN complex recruitment [3]. In allergic rhinitis, TRIM24-conditional knockout (CKO) mice in CD4+ T cells have more severe AR symptoms with enhanced Th2 polarization due to decreased STAT6 acetylation [5].

In conclusion, Trim24 KO/CKO mouse models have revealed its crucial roles in macrophage polarization, DNA repair, and allergic rhinitis. Trim24 is important in regulating these biological processes, and its dysregulation is associated with tumor progression and allergic diseases, providing potential therapeutic targets.