Hdac10, histone deacetylase 10, is a class-IIb HDAC involved in multiple biological processes. It is crucial for gene regulation by modifying histone acetylation, which impacts chromatin structure and gene expression. It also participates in various pathways related to immunity, inflammation, and cell growth, thus being of great biological importance. Genetic models, such as KO/CKO mouse models, are valuable for studying its functions.

In asthma, Hdac10-deficient (Hdac10fl/fl-LysMCre) mice showed protection from airway inflammation. Hdac10 deficiency attenuated STAT3 expression and decreased M2 macrophage polarization, suggesting that HDAC10 promotes airway inflammation by interacting with STAT3 to regulate macrophage polarization [1]. In melanoma, depletion or inhibition of HDAC10 upregulated SPARC expression, repressed cell growth, and resensitized resistant cells to BRAF inhibitors [2,5]. In lung adenocarcinoma, Hdac10 deletion accelerated tumor development, increased macrophage infiltration, and enhanced the presence of cancer stem-like cells [4]. In T-regulatory (Treg) cells, HDAC10 -/- Treg exhibited increased suppressive function, protecting mice from colitis and promoting allograft tolerance in cardiac transplantation [3]. In cervical cancer, HDAC10 was poorly expressed and inhibited cancer progression by down-regulating the HDAC10-microRNA-223-EPB41L3 axis [6]. In antiviral innate immune responses, HDAC10 deficiency in mouse embryonic fibroblasts and mice promoted the expression of type I IFNs and ISGs, enhancing antiviral responses [7].

In summary, Hdac10 plays essential roles in various biological processes and diseases. Studies using KO/CKO mouse models have revealed its significant impact on asthma, melanoma, lung adenocarcinoma, colitis, cervical cancer, and antiviral immunity, providing insights into potential therapeutic strategies for these diseases.