POU2AF1, also known as OCA-B, is a transcription co-factor. It plays diverse roles in multiple biological processes. It is involved in pathways related to cell differentiation, immune response regulation, and adipogenesis. Its functions are crucial for normal physiological activities and its dysregulation may lead to various diseases [1,2,3,5,6,7].

In overweight patients, POU2AF1 expression is upregulated in retroperitoneal adipose tissue and promotes mesenchymal stem cells (MSCs) adipogenesis by inhibiting HDAC1 expression. Silencing endogenous POU2AF1 in MSCs inhibits adipogenesis [2]. In the context of Tfh cell maturation, Pou2af1 promotes Tfh formation and migration into the germinal center by upregulating CXCR5 [3]. In B-cell malignancies, B-cell malignancies dependent on POU2AF1 are sensitive to mSWI/SNF ATPase degraders, with treatment leading to chromatin eviction of POU2AF1 [4]. In CD4+ T cells, ectopic OCA-B (POU2AF1) expression improves antiviral memory recall responses and endogenously elevated OCA-B expression can prospectively identify memory precursor cells [5]. In the human airway epithelium, POU2AF1 helps maintain a host defense tone by regulating host-defense genes, and its expression is suppressed by cigarette smoke [6]. In chronic obstructive pulmonary disease (COPD), POU2AF1 may be a key regulator of emphysema, contributing to disease progression by regulating B-cell immunology [7].

In summary, POU2AF1 is a multifunctional transcription co-factor involved in adipogenesis, immune cell regulation, and host defense. Studies, including those using gene-knockout or conditional-knockout models in some cases, have revealed its role in diseases such as adiposity-related conditions, certain malignancies, and respiratory diseases, providing insights into potential therapeutic targets.