Interleukin 10 (IL-10) is a cytokine with a wide range of biological activities, secreted by antigen-presenting cells such as activated T cells, monocytes, B cells, and macrophages. IL-10 plays a pleiotropic role in immunoregulation and inflammation, downregulating the expression of Th1 cytokines, MHC class II antigens, and co-stimulatory molecules on macrophages, and enhancing the survival, proliferation, and antibody production of B cells. IL-10 can block NF-kB activity and participate in the regulation of the JAK-STAT signaling pathway. In addition, IL-10 can also activate PI3K and its downstream substrates p70S6K and Akt/PKB. Overexpression of IL-10 (such as in systemic lupus erythematosus, tuberculosis) and IL-10 deficiency (such as in inflammatory bowel disease, psoriasis, asthma, rheumatoid arthritis) have different pathophysiological significance. Therefore, neutralizing cytokines may be an effective method for treating the former group of diseases, while the application of IL-10 itself may help treat the latter group of diseases. This strain is an Il10 gene knockout (Il10 KO) mouse, in which the Il10 gene homologous to the human IL10 gene has been knocked out in mice using gene editing technology. Homozygous Il10-KO mice do not produce the anti-inflammatory cytokine IL-10 and can survive and reproduce under specific pathogen-free (SPF) conditions. This strain is maintained in a high-standard SPF environment in Cyagen facilities, and its phenotype differs from that of Il10 knockout mice raised in conventional mouse facilities as reported in the literature. For example, the development of colitis in this model may be slow or non-spontaneous, but the introduction of microbes or fecal microbiota may cause rapid development of colitis in adult animals. Homozygous Il10 KO mice are viable and fertile.

Interleukin-10 (IL-10) is a cytokine secreted by activated T cells, monocytes, B cells, and macrophages, among other antigen-presenting cells. It exhibits broad biological activity. In immune regulation and inflammatory responses, IL-10 can reduce the expression of Th1 cytokines, MHC-II antigens, or co-stimulatory molecules. Simultaneously, it enhances B cell survival, proliferation, and antibody production. Both overexpression (as seen in systemic lupus erythematosus and tuberculosis) and deficiency (as observed in inflammatory bowel disease, psoriasis, asthma, and rheumatoid arthritis) of IL-10 have pathological and physiological significance. IL-10 is a critical susceptibility gene for inflammatory bowel disease (IBD), and its functional defects play a central role in the development of ulcerative colitis (UC)-type IBD ^[1]. The genetic polymorphism of IL-10 may also contribute to the occurrence of UC-type IBD or Crohn’s disease (CD)-type IBD ^[2]. Therefore, IL-10 gene knockout mice exhibit a phenotype similar to human inflammatory bowel disease (IBD) and are widely used in research related to relevant diseases ^[3]. During the gene editing process, using different mouse strain backgrounds may lead to differences in disease phenotypes. BALB/c strain and C57BL/6 strain exhibit significant differences in susceptibility to infection, resistance, and immune deficiencies. For specific applications such as evaluating antifungal drug efficacy, cancer treatment, and immunological research, the BALB/c strain has its unique advantages ^[4-6]. Research has found that IL-10-deficient BALB/c mice are more susceptible to colitis than mice of the C57BL/6 strain. Additionally, the disease phenotype is more severe in IL-10-deficient BALB/c mice, making them a more effective model for simulating the disease progression of human colitis ^[7]. This model is Il10 gene knockout mice, where the Il10 gene homologous to the human IL10 gene has been knocked out in BALB/cAnCya mice. Homozygous BALB/c-Il10 KO mice are viable and fertile. At 8 to 9 weeks of age, BALB/c-Il10 KO mice spontaneously develop colitis symptoms, characterized by weight loss, reduced survival rates, elevated levels of inflammatory factors, and abnormalities in intestinal inflammation and phenotype. BALB/c-Il10 KO mice can be used for research related to Crohn’s disease (CD), colitis, other inflammatory bowel diseases (IBD), cancer, congenital and adaptive immune disorders, as well as various inflammation or autoimmune conditions. It should be noted that due to individual variability and environmental factors, the disease presentation of this model may vary. The data in this manual are based on internal facility observations and are provided for reference. Actual disease presentation may vary; please use the mice according to your specific experimental conditions for best results.

Aurkb is located on chromosome 11 of mice. Nuclease Technology was used to design sgRNA; Aurkb knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Il10 is located on chromosome 1 of mice. Nuclease Technology was used to design sgRNA; Il10 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Il10 is located on chromosome 1 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Il10 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.

Zcchc13 is located on chromosome X of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Zcchc13 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.