The IL22 gene encodes the protein interleukin-22, a cytokine of the IL-10 family. This gene is primarily expressed in immune cells, such as T helper 17 (Th17) cells, Th22 cells, and innate lymphoid cells (ILCs), which then produce and secrete the IL-22 protein ^[1]. Unlike most cytokines, which primarily act on immune cells, IL-22's primary targets are non-hematopoietic cells, specifically the epithelial and stromal cells that form the body's barrier tissues. IL-22 receptor is most notably found in tissues such as the skin, lungs, gastrointestinal tract, liver, and pancreas. The protein's dual function includes promoting antimicrobial defense and tissue repair by inducing proliferation and inhibiting apoptosis in these epithelial cells ^[2]. However, its dysregulation is associated with both inflammatory and protective roles in a variety of diseases. High levels of IL-22 are linked to autoimmune conditions like psoriasis, rheumatoid arthritis (RA), and inflammatory bowel disease (IBD), as well as some cancers, while in other contexts, it can be protective, aiding in the recovery from infections and tissue damage ^[3]. The B6-huIL22 mouse is a humanized model constructed via gene-editing technology. The sequence from the ATG start codon to the TGA stop codon of mouse Il22 will be replaced with the sequence from the ATG start codon to the TGA stop codon of human IL22. B6-huIL22 mice can be used for research into the pathogenesis of autoimmune disorders like psoriasis, rheumatoid arthritis (RA), and inflammatory bowel disease (IBD), as well as some cancers and infections, and for the screening, development, and safety evaluation of IL22-targeted drugs.