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. The homozygous mice are viable and fertile.