The A129 (Ifnar1 KO) mice on a 129 background are a type I (α/β) interferon receptor (Ifnar1) gene knockout model. The absence of the IFNAR1 protein in these mice leads to a lack of type I IFN receptor function, thereby reducing immune response and increasing susceptibility to viral infections. Homozygous A129 (Ifnar1 KO) mice are viable and fertile, but they show increased susceptibility to arbovirus infections.

The IFNAR1 gene encodes a key component of the type I IFN receptor, while the IFNGR1 gene encodes the ligand-binding chain (α) of the type II (γ) IFN receptor. AG129 mice, which are knockout models for both the type I (α/β) IFN receptor (Ifnar1) and the type II (γ) IFN receptor (Ifngr1), lack functional IFNAR1 and IFNGR1 proteins, resulting in deficiencies in α/β/γ interferon receptor signaling and heightened susceptibility to viral infections. Homozygous AG129 mice are viable and fertile, and exhibit increased sensitivity to arboviral infections, generating viremia similar to that seen in humans. Compared to IFNα/β/γR KO mice on the C57BL/6 background, the 129-background AG129 mice exhibit more pronounced neurological symptoms after infection.

This strain is a mouse Alox5 gene deletion model, achieved by using gene editing technology to knock out the homologous gene of human ALOX5 in mice. According to literature reports, these mice exhibit increased total adipose tissue weight, plasma VLDL/LDL cholesterol, and bone mineral density. Their spleens are typically smaller than those of wild-type mice, and they exhibit reduced inflammatory responses and abnormalities in immunophysiology. These homozygous Alox5 KO mice are viable and fertile.

The mouse Ighg1 gene is homologous to the human IGHG1, IGHG2, and IGHG3 genes. B6-IgG1 KO mice are constructed by knocking out the Ighg1 gene in mice, creating a model of IgG1 deficiency. This model provides an effective tool for research on diseases related to IgG1 deficiency.

The B6-IgA KO mouse is an IgA-deficient model developed by knocking out the mouse Igha gene, which encodes IgA, in mice. This mouse model provides a valuable tool for studying diseases associated with selective IgA deficiency.

This strain is an Ighj-deletion model, in the homozygous B6-Ighj KO mice, the J-segment of the Ig heavy chain locus is completely deleted, resulting in the inability of the cell to produce a recombinant version of the complete heavy chain variable region. The B cells of B6-Ighj KO mice have undergone dramatic changes in the developmental process and cell number, which can be used as an animal model of B-cell immune deficiency. B6-Ighj KO mice retain other immune cells except for B cells, so the presence of other immune cells can be detected in B6-Ighj KO mice.

This strain is an Ighm-deletion model and the homozygous mice lack mature B cells, develop normally and fertile.

The B6-Igl KO mouse is a knockout model targeting the gene segment encoding the λ light chain. Through gene editing, the sequences encoding the V, J, and C regions of the mouse λ light chain (Igl) locus are completely ablated, resulting in the absence of B cells expressing immunoglobulin light chain λ. Consequently, B6-Igl KO mice serve as a valuable tool for investigating B cell development and function, generating κ light chain-only mouse antibodies, elucidating the role of the λ light chain in specific immune responses or autoimmune diseases, and exploring antibody diversity, immune regulatory mechanisms, and potential therapeutic strategies.

B6-Il2rg KO mice were obtained by knocking out the expression of the Il2rg gene in C57BL/6JCya mice, which are severely deficient in B and T cells in peripheral blood and bone marrow and partially deficient in the spleen, while the mice show a severe immunodeficient phenotype with almost complete absence of NK cells in peripheral blood, spleen, and bone marrow. This strain can be used for research in the fields of oncology, immunology, infectious disease, and stem cell biology.

This strain is a Tcra gene deletion model in which homozygous B6-Tcra KO mice with αβ T-cell receptor deficiency have thymuses lacking CD4+CD8- and CD4-CD8+ cells, and approximately 1.5% of thymocytes express γδ T-cell receptors. homozygous B6-Tcra KO mice are developmentally normal and fertile, but mortality increases after 6 months, and few mice survive beyond one year.