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.

B6-H11-hCLEC4C mice are humanized models generated by gene editing technology, in which the human CLEC4C genomic DNA was inserted at the H11 safe harbor. This modification does not affect the expression of the mouse homologous gene Clec4b1. This model can be used to study the pathological mechanisms and therapeutic methods of autoimmune disorders and hematological malignancies, as well as the screening and development of CLEC4C-targeted drugs, and preclinical efficacy and safety evaluations.

The B6-h4-1BB (TNFRSF9) mouse is a humanized model. The sequence encoding the endogenous extracellular domain of the mouse Tnfrsf9 is replaced in situ with the sequence encoding the human TNFRSF9 extracellular domain. This model can be used for studies on cancer immunology and autoimmune diseases, as well as for the development, screening, and evaluation of 4-1BB agonists in preclinical research.

B6-h4-1BB/hPDL1 mice are TNFRSF9 and CD274 double humanized mouse models obtained by mating TNFRSF9 humanized mouse models (Catalog No. C001604) with CD274 humanized mouse models (Catalog No. C001235). They express human TNFRSF9 and CD274 genomic sequences under the control of mouse promoters. This model is a valuable tool for studying cancer immunotherapy. In addition, this model also provides a powerful preclinical research platform for evaluating the efficacy and mechanism of therapeutic drugs targeting TNFRSF9 and CD274.

The B6-hB2M&HLA-A2.1/mB2m KO mice are a humanized model obtained by mating H11-hB2M&HLA-A2.1 mice (Catalog Number: I001138) with B2m gene knockout mouse model (Catalog Number: S-KO-19919). While knocking out the mouse B2m gene, the chimeric H2-K1 HLA-A2.1 gene is integrated into the H11 safe harbor locus, which may be able to recapitulate the immune response of the human HLA-A*0201 (MHCI) subtype. This model can play an important role in studying the determinants of HLA-A2.1-restricted cytotoxic T lymphocytes (CTLs) and the development of potential viral vaccines and helps research the human immune response to a variety of antigens.

The B6-hBAFF (TNFSF13B) mouse is a humanized model generated using gene editing technology, in which the protein-coding sequence (CDS) encoding the extracellular domain of the human TNFSF13B protein is integrated into a specific site within the mouse Tnfsf13b gene, while retaining the endogenous gene sequence encoding the mouse cytoplasmic and transmembrane domains (aa.1-68). Homozygous B6-hBAFF (TNFSF13B) mice are viable and fertile. This model can be used for studying the pathological mechanisms and therapeutic approaches of autoimmune diseases and specific B cell malignancies and for the development of BAFF-targeted drugs.

The B6-hBAFFR (hTNFRSF13C) mouse is a humanized model constructed by replacing the sequence of the mouse Tnfrsf13c endogenous extracellular domain (aa.1~71) in situ with the corresponding extracellular domain (aa.1~78) from the human TNFRSF13C. The B6-hBAFFR (hTNFRSF13C) mice can be used for the study of the pathogenesis of immune-mediated disorders such as common variable immunodeficiency (CVID), systemic lupus erythematosus (SLE), and Sjögren's syndrome, and certain B cell malignancies, as well as for TNFRSF13C-targeted drug development.

The B6-hBCMA (TNFRSF17) mouse is a humanized model constructed using gene editing technology, where the mouse BCMA endogenous extracellular domain (aa.1~49) was replaced with the human BCMA extracellular domain (aa.1~54). Homozygous B6-hBCMA (TNFRSF17) mice are viable and fertile. This model can be used for studying the pathological mechanisms and therapeutic approaches of multiple myeloma, systemic lupus erythematosus and various B cell-related diseases and for the development of BCMA-targeted drugs.

The B6-hC3 mouse is a mouse C3 humanized model created by replacing the mouse C3 gene with the human C3 gene using gene-editing technology. The humanized regions include the 5’UTR and 3’UTR. Under natural breeding conditions, homozygous B6-hC3 mice exhibit mortality around 10 weeks of age, and it has been observed that heterozygous mice also experience mortality.