The IL23A gene encodes the p19 subunit, a component of interleukin-23 (IL-23), which forms a heterodimer with the p40 subunit (encoded by IL12B) to generate the functional IL-23 cytokine ^[1]. Primarily expressed by activated dendritic cells, macrophages, and monocytes, IL-23 signals through the IL-23 receptor (IL-23R) complex, activating the JAK-STAT pathway to promote Th17 cell differentiation and maintain IL-17 production. This process drives inflammatory responses and mucosal immunity against extracellular pathogens ^[1-2]. Genetic polymorphisms within IL23A are strongly associated with autoimmune and inflammatory diseases, including psoriasis, Crohn's disease, and inflammatory bowel disease, due to dysregulated Th17 activity and chronic inflammation ^[1-2]. Monoclonal antibodies targeting IL-23, such as risankizumab and guselkumab, selectively block the p19 subunit, demonstrating therapeutic efficacy in psoriasis and inflammatory bowel diseases by suppressing pathogenic IL-17/Th17 pathways ^[3]. While IL-23 plays a role in protective immunity, its overactivation contributes to tissue damage in autoimmune settings, highlighting its dual function in immune regulation and disease pathogenesis ^[1-4].

The B6-hIL23A mouse is a humanized model generated by gene editing, in which the mouse Il23a genomic sequence is replaced with the corresponding sequence from the human IL23A gene, while preserving the endogenous sequence encoding the mouse IL23p19 signal peptide. Homozygous B6-hIL23A mice are viable and fertile, and suitable for investigating the pathomechanisms and therapeutic interventions of immune-related diseases and cancer, as well as for screening and developing IL23A-targeted therapeutics, and for preclinical pharmacodynamic and safety evaluations.