Il12a KO Mouse

The interleukin 12A (IL12A or IL12p35) gene encodes the subunits of cytokines IL-12 and IL-35, which act on T cells and natural killer (NK) cells and have extensive biological activity. IL-12 is a heterodimer composed of the p35 subunit encoded by the IL12A gene and the p40 subunit, a member of the cytokine receptor family encoded by the IL12B gene. It is essential for non-T cell-dependent interferon-gamma (IFN-γ) induction and is also crucial for the differentiation of helper T cells (Th1 and Th2). On the other hand, the primary function of IL-35 is to suppress the inflammatory response of immune cells. IL12A also affects cardiovascular diseases by regulating inflammation, including heart fibrosis and myocardial infarction. Mutations in the IL12A gene are associated with susceptibility to certain infectious and autoimmune diseases^[1].

This model is an Il12a gene knockout mouse, created using gene-editing technology to knock out the homologous Il12a gene of the human IL12A gene in mice. According to the literature, the deletion of Il12a in this mouse model leads to the loss of the biological effects of IL-12 and IL-35, reduced NK cell responses, altered differentiation of effector T cells, and increased susceptibility to parasitic infections. Additionally, this model cannot exhibit delayed-type hypersensitivity (DTH) reactions induced by the interaction of effector T cells with antigens^[2]. The homozygous mice are viable and fertile.