B6-hBAFF/huAPRIL Mouse
Product Name
B6-hBAFF/huAPRIL Mouse
Product ID
C001802
Strain Name
C57BL/6NCya-Tnfsf13bem1(hTNFSF13B)Tnfsf13tm1(hTNFSF13)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “B6-hBAFF/huAPRIL Mouse (Catalog C001802) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Alias
APRIL, CD256, TALL2, ZTNF2, TALL-2, TNLG7B, TRDL-1, UNQ383/PRO715, DTL, BAFF, BLYS, CD257, TALL1, THANK, ZTNF4, TALL-1, TNLG7A, TNFSF20
Chromosome
Chr 17, Chr 13
MGI ID
Datasheet
Strain Description
The TNFSF13B gene encodes B cell-activating factor (BAFF), a critical cytokine for B cell survival and maturation, primarily expressed by monocytes, macrophages, dendritic cells, and T cells [1]. BAFF, a member of the tumour necrosis factor (TNF) superfamily, functions through binding to receptors on B cells, including BAFF-R, TACI, and BCMA. Activation of these receptors initiates the NF-κB and MAPK signaling cascades, leading to B cell survival, proliferation, and immunoglobulin production [1-2]. This cytokine is essential for humoral immunity and the development of lymphoid tissues [1]. Aberrant BAFF expression and signaling are implicated in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. BAFF overexpression can drive B cell hyperactivity and the production of autoantibodies, contributing to these conditions [2-3]. Clinically, monoclonal antibodies targeting BAFF, such as belimumab, are employed in the treatment of SLE [4]. In the tumor microenvironment, BAFF exhibits a complex role, supporting B cell lymphomas and influencing the immune response to solid tumours, exhibiting context-dependent pro- and anti-tumourigenic effects [5]. This multifaceted role highlights BAFF as a key therapeutic target in autoimmune diseases and specific B cell malignancies [1-5].
The TNFSF13 gene, also known as APRIL (a proliferation-inducing ligand), encodes a critical member of the tumor necrosis factor (TNF) superfamily. Its expression is detected in various cell types within the immune and stromal compartments, including monocytes, macrophages, dendritic cells, and bone marrow precursors [6]. The encoded cytokine functions by binding to specific receptors, namely TNFRSF17/BCMA and TNFRSF13B/TACI, thereby regulating key aspects of B cell and plasma cell biology, including their development and long-term survival. TNFSF13 is instrumental in the adaptive immune response, facilitating antibody class switching and providing essential survival cues to antibody-secreting cells [7]. Dysregulated TNFSF13 expression has been etiologically linked to various pathologies. Aberrant TNFSF13 signaling contributes to the pathogenesis of multiple myeloma and chronic lymphocytic leukemia (CLL) by promoting the proliferation and survival of malignant cells [8]. Furthermore, its dysregulation is also implicated in the progression of several autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) [9].
The B6-hBAFF/huAPRIL mouse is a dual-gene humanized model generated by crossing B6-hBAFF (hTNFSF13B) mice (Catalog No.: C001621) with B6-huAPRIL (huTNFSF13) mice (Catalog No.: C001852). This model can be used for the study of autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) and B cell malignancies, as well as for the development of related targeted therapeutics.
Reference
Smulski CR, Eibel H. BAFF and BAFF-Receptor in B Cell Selection and Survival. Front Immunol. 2018 Oct 8;9:2285.
Huang T, Pi C, Xu X, Feng Y, Zhang J, Gu H, Fang J. Effect of BAFF blockade on the B cell receptor repertoire and transcriptome in a mouse model of systemic lupus erythematosus. Front Immunol. 2024 Jan 9;14:1307392.
Giordano D, Kuley R, Draves KE, Elkon KB, Giltiay NV, Clark EA. B cell-activating factor (BAFF) from dendritic cells, monocytes and neutrophils is required for B cell maturation and autoantibody production in SLE-like autoimmune disease. Front Immunol. 2023 Feb 27;14:1050528.
Ramsköld D, Parodis I, Lakshmikanth T, Sippl N, Khademi M, Chen Y, Zickert A, Mikeš J, Achour A, Amara K, Piehl F, Brodin P, Gunnarsson I, Malmström V. B cell alterations during BAFF inhibition with belimumab in SLE. EBioMedicine. 2019 Feb;40:517-527.
Ullah MA, Mackay F. The BAFF-APRIL System in Cancer. Cancers. 2023; 15(6):1791.
Chen R, Wang X, Dai Z, Wang Z, Wu W, Hu Z, Zhang X, Liu Z, Zhang H, Cheng Q. TNFSF13 Is a Novel Onco-Inflammatory Marker and Correlates With Immune Infiltration in Gliomas. Front Immunol. 2021 Oct 12;12:713757.
Poznyak AV, Gerasimova EV, Orekhov NA, Karimova AE, Vergun MA, Lapshina KO, Sukhorukov VN, Orekhov AN. Exploring the role of APRIL in autoimmunity: implications for therapeutic targeting in systemic lupus erythematosus, rheumatoid arthritis, and Sjögren's syndrome. Front Immunol. 2025 Aug 1;16:1523392.
Ullah MA, Mackay F. The BAFF-APRIL System in Cancer. Cancers (Basel). 2023 Mar 16;15(6):1791.
Muto M, Suzuki H, Suzuki Y. New Insights and Future Perspectives of APRIL in IgA Nephropathy. Int J Mol Sci. 2024 Sep 26;25(19):10340.
Strain Strategy
Figure 1. Gene editing strategy of B6-hBAFF(TNFSF13B) mice. The region from aa.69 in exon 1 to partial intron 1 of mouse Tnfsf13b was replaced with Human TNFSF13B CDS of extracellular domain-WPRE-BGH pA cassette. The murine cytoplasmic and transmembrane domain was preserved.
Figure 2. Gene editing strategy of B6-huAPRIL (huTNFSF13) mice. The sequences from the ATG start codon to the TGA stop codon of the endogenous mouse Tnfsf13 gene were replaced with the sequences from the ATG start codon to the TGA stop codon of the human TNFSF13 gene. The Neo cassette was inserted downstream of the TGA stop codon. The function of the mouse Tnfsfm13 and Tnfsf13os genes will be affected.
Application Area
Research on the pathological mechanisms and therapeutic approaches of autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE);
Research on the pathological mechanisms and therapeutic approaches of specific B cell malignancies.
Contact Us
Connect with our experts for your custom animal model needs. Please fill out the form below to start a conversation or request a quote.
Cyagen values your privacy. We’d like to keep you informed about our latest offerings and insights. Your preferences:
You may unsubscribe from these communications at any time. See our Privacy Policy for details on opting out and data protection.
By clicking the button below, you consent to allow Cyagen to store and process the personal information submitted in this form to provide you the content requested.