The Arachidonate 5-lipoxygenase (ALOX5) gene encodes 5-Lipoxygenase (5-LO), a key member of the fatty acid oxidase gene family. 5-LO is one of the crucial enzymes in the metabolic pathway of arachidonic acid (AA), an essential fatty acid in humans. It catalyzes the conversion of AA into leukotrienes (LTs), which are important mediators of various inflammatory and allergic diseases. ALOX5 is specifically expressed in bone marrow-derived cells and is significantly upregulated in myeloid leukemia stem cells, playing a pivotal role in the development of myeloid leukemia. Mutations in the promoter region of this gene weaken the response to leukotriene antagonists used for asthma treatment and are also associated with atherosclerosis and some cancers. Multiple splice variants encoding different isoforms have been identified for this gene. 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^[1-3]. These homozygous Alox5-KO mice are viable and fertile.

Interferons (IFNs) are potent cytokines that serve as a critical component of the body's first line of defense against viral infections, playing a key role in inflammation and immune control by directly inducing pathogen-inhibiting molecules that suppress viral replication ^[1]. Arthropod-borne viruses (arboviruses) like Dengue virus (DENV), Zika virus (ZIKV), and Yellow Fever virus (YFV) encode proteins that antagonize the IFN response, helping these viruses evade host immunity and maintain sufficient viral loads in the blood (viremia) to sustain the vector-host transmission. Arboviruses pose a significant public health threat, affecting around 3.9 billion people in tropical and subtropical regions. However, most preclinical studies suggest that arboviruses cannot inhibit IFN responses in mice, rendering immunocompetent mice resistant to infection, with low viral loads and limited circulation, thus limiting their use in infection research ^[2-3]. As a result, immunodeficient mouse models with defects in multiple IFN signaling pathways have become essential tools for studying arbovirus pathogenesis and vaccine development ^[2-4]. Studies have demonstrated that wild-type mice of strains like C57BL/6, CD-1, or 129 rarely exhibit clinical symptoms after infection with arboviruses such as ZIKV. However, the virus has been detected in the blood, ovaries, and spleen of ZIKV-infected 129 mice, suggesting that this strain may be more susceptible to arboviruses ^[5-6]. Because the virus can persist in the bloodstream without causing disease or death, the 129 strain can be used to evaluate the teratogenic effects of such viruses. Furthermore, the 129 strain is commonly used in interferon signaling-deficient models related to other viral infections ^[7-8]. 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(IFNα/β/γR-DKO) 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(IFNα/β/γR-DKO) 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(IFNα/β/γR-DKO) mice exhibit more pronounced neurological symptoms after infection ^[6,9].

Interferons (IFNs) are potent cytokines that serve as a critical component of the body's first line of defense against viral infections, playing a key role in inflammation and immune control by directly inducing pathogen-inhibiting molecules that suppress viral replication ^[1]. Arthropod-borne viruses (arboviruses) like Dengue virus (DENV), Zika virus (ZIKV), and Yellow Fever virus (YFV) encode proteins that antagonize the IFN response, helping these viruses evade host immunity and maintain sufficient viral loads in the blood (viremia) to sustain the vector-host transmission. Arboviruses pose a significant public health threat, affecting around 3.9 billion people in tropical and subtropical regions. However, most preclinical studies suggest that arboviruses cannot inhibit IFN responses in mice, rendering immunocompetent mice resistant to infection, with low viral loads and limited circulation, thus limiting their use in infection research ^[2-3]. As a result, immunodeficient mouse models with defects in multiple IFN signaling pathways have become essential tools for studying arbovirus pathogenesis and vaccine development ^[2-4]. Studies have demonstrated that wild-type mice of strains like C57BL/6, CD-1, or 129 rarely exhibit clinical symptoms after infection with arboviruses such as ZIKV. However, the virus has been detected in the blood, ovaries, and spleen of ZIKV-infected 129 mice, suggesting that this strain may be more susceptible to arboviruses ^[5-6]. Because the virus can persist in the bloodstream without causing disease or death, the 129 strain can be used to evaluate the teratogenic effects of such viruses. Furthermore, the 129 strain is commonly used in interferon signaling-deficient models related to other viral infections ^[7-8]. The IFNAR1 gene encodes a protein that is an essential component of the type I interferon (IFN) receptor, playing a critical role in the antiviral and immune responses. IFNAR1 is primarily expressed in immune cells, such as lymphocytes and dendritic cells, and various tissues, including the liver, brain, and skin. Defects in IFNAR1, whether due to mutations or regulatory abnormalities, can lead to severe diseases such as systemic lupus erythematosus, where excessive immune activation results in tissue damage, and certain cancers. Other diseases associated with IFNAR1 include hepatitis C, yellow fever, measles, papilloma, and viral infections. 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.

Immunoglobulins recognize foreign antigens and initiate immune responses such as phagocytosis and the complement system. Each immunoglobulin molecule consists of two identical heavy chains and two identical light chains. Immunoglobulin heavy locus, also known as IGH, is a region that contains a gene for the heavy chains of human antibodies (or immunoglobulins), this locus includes V (variable), D (diversity), J (joining), and C (constant) segments. During B cell development, a recombination event at the DNA level joins a single D segment with a J segment; the fused D-J exon of this partially rearranged D-J region is then joined to a V segment. The rearranged V-D-J region containing a fused V-D-J exon is then transcribed and fused at the RNA level to the IGHM constant region; this transcript encodes a mu-heavy chain. Later in development B cells generate V-D-J-Cmu-Cdelta pre-messenger RNA, which is alternatively spliced to encode either a mu or a delta-heavy chain. Mature B cells in the lymph nodes undergo switch recombination so that the fused V-D-J gene segment is brought in proximity to one of the IGHG, IGHA, or IGHE gene segments and each cell expresses either the gamma, alpha, or epsilon heavy chain.
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.

The IL2RG gene encodes the interleukin-2 receptor gamma chain (IL-2Rγ), also known as the common gamma chain (γc). This receptor subunit is shared by several immune factors, including IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. When these cytokines bind to their receptors, they promote cell growth and division. Mutations in the IL2RG gene can lead to X-linked severe combined immunodeficiency (X-SCID), a condition characterized by a lack of T cells and natural killer cells, and non-functional B cells. As a result, patients with X-SCID are highly susceptible to recurrent infections and are unable to survive beyond infancy ^[1-2]. In mice, knockout of the Il2rg gene leads to severe depletion of B cells, T cells, and NK cells ^[2]. The RAG2 gene encodes a protein that forms the RAG complex with the RAG1 protein. This complex plays a crucial role in V(D)J recombination during B and T cell maturation. The RAG complex attaches to a section of DNA called a recombination signal sequence (RSS), next to a V, D, or J segment, and makes small cuts in the DNA so that the segment can be separated and moved. This process is repeated multiple times in different areas within B cells and T cells so that the V, D, and J segments are arranged in various combinations, providing greater recognition of foreign invaders ^[3]. A lack of functional RAG2 protein can lead to SCID. In mice, deletion of the Rag2 gene leads to loss of V(D)J recombination, resulting in blocked differentiation, development, and maturation of T cells and B cells ^[4]. BRG mice are models with the double knockout of Il2rg and Rag2 genes. This model presents more severe depletion of B cells, T cells, and NK cells as well as other severe combined immunodeficiency phenotypes than mice with knockout of either the Il2rg or Rag2 genes alone ^[5]. BRG mice can be used for research in various fields of oncology and immunology.

Surface membrane immunoglobulin (SmIg) of the B cell membrane is a receptor that specifically recognizes antigens of B cells, and it is also an important characteristic marker of B cells. Early immature B cells express immunoglobulin M (IgM), while mature B cells express both membrane IgM (mIgM) and membrane IgD (mIgD). This strain is a mouse Ighm gene and Ighd gene double knockout model. Homozygous BALB/c-Ighm Ighd-DKO mice lack mature B cells and can be used as an animal model of B cell immunodeficiency.

Surface membrane immunoglobulin (SmIg) of the B cell membrane is a receptor that specifically recognizes antigens of B cells, and it is also an important characteristic marker of B cells. Early immature B cells express immunoglobulin M (IgM), while mature B cells express both membrane IgM (mIgM) and membrane IgD (mIgD). This strain is a mouse Ighm gene and Ighd gene double knockout model. Homozygous B6J-Ighm Ighd-DKO mice lack mature B cells and can be used as an animal model of B cell immunodeficiency.

Immunoglobulin M (IgM) is a basic antibody secreted by B cells and is by far the largest antibody found in the human circulatory system, and the first to react to antigens, with the spleen being the largest producer of IgM. Due to its extremely large molecular weight, IgM is very effective in antigen agglutination reactions. In the early stages of B-cell-mediated (humoral) immunity, IgG is not sufficient and IgM is primarily responsible for the clearance of pathogens. As the first circulating antibody to respond to the initial encounter with a foreign antigen, IgM concentration in the blood decreases rapidly due to clearance, and therefore, Immature B cells begin to express membrane IgM (mIgM), but the BCR of immature B cells that express only mIgM can react with membrane self-antigens on the surface of bone marrow cells to block the differentiation of the cells into mature B cells, which is one of the mechanisms by which autoimmune tolerance develops. This strain is an Ighm-deletion model, and the homozygous mice lack mature B cells but develop normally and are fertile.

Immunoglobulin M (IgM) is a basic antibody secreted by B cells and is by far the largest antibody found in the human circulatory system and the first to react to antigens, with the spleen being the largest producer of IgM. Due to its extremely large molecular weight, IgM is very effective in antigen agglutination reactions. In the early stages of B-cell-mediated (humoral) immunity, IgG is not sufficient and IgM is primarily responsible for the clearance of pathogens. As the first circulating antibody to respond to the initial encounter with a foreign antigen, IgM concentration in the blood decreases rapidly due to clearance, and therefore, Immature B cells begin to express membrane IgM (mIgM), but the BCR of immature B cells that express only mIgM can react with membrane self-antigens on the surface of bone marrow cells to block the differentiation of the cells into mature B cells, which is one of the mechanisms by which autoimmune tolerance develops. This strain is an Ighm-deletion model, and the homozygous mice lack mature B cells but develop normally and are fertile.

The interleukin-2 receptor subunit gamma (IL2Rg or CD132) gene encodes a protein that is an important signaling component of many interleukin receptors and is a common receptor subunit for several important immune factors, including IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. IL2Rg is a glycoprotein expressed on the surface of most lymphocytes. In mammals, the IL2Rg gene is located on the X chromosome, and mutations in IL2Rg in humans can lead to X-linked severe combined immunodeficiency (X-SCID). 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.