Arid5a, also known as AT-rich interactive domain 5A, is a nucleic acid binding protein with dual functions as a transcription factor co-factor and an RNA-binding protein [1,3,5]. It contributes to cell growth, differentiation, and is involved in regulating processes like immune regulation, inflammation, and cellular homeostasis. It can bind to the 3' untranslated region (UTR) of mRNAs such as Il-6, stabilizing them and influencing inflammatory responses [6].

In various in vivo studies using gene knockout (KO) mouse models, Arid5a has been shown to have significant impacts. Arid5a-/-mice were refractory to autoantibody-induced glomerulonephritis (AGN), with attenuated myeloid infiltration and impaired expression of IL-17-dependent cytokines and transcription factors, indicating its role in IL-17-dependent renal autoimmunity [4]. In lung cancer, β-catenin-mediated transcriptional regulation of FOSL2 and Arid5a drives the gene regulatory switch from M1-like to M2-like tumor-associated macrophages (TAMs), influencing tumor progression [2]. In addition, deletion of Arid5a in tumor cell lines enhanced antitumor immunity in immunocompetent mice, suggesting its role in immune evasion [7].

In conclusion, Arid5a plays multifaceted roles in immune regulation, inflammation, and cancer. The use of Arid5a KO mouse models has revealed its importance in diseases such as autoantibody-induced glomerulonephritis, lung cancer, and in the context of tumor immune evasion. Understanding Arid5a's functions provides potential therapeutic targets for treating inflammatory and autoimmune disorders as well as cancer [1,3,5].