B6-hBAFFR (hTNFRSF13C) Mouse
Product Name
B6-hBAFFR (hTNFRSF13C) Mouse
Product ID
C001711
Strain Name
C57BL/6NCya-Tnfrsf13ctm1(hTNFRSF13C)/Cya
Backgroud
C57BL/6NCya
When using this mouse strain in a publication, please cite “B6-hBAFFR (hTNFRSF13C) Mouse (Catalog C001711) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
Gene Alias
BAFFR, CD268, CVID4, BAFF-R, BROMIX, prolixin
NCBI ID
Chromosome
Chr 22
MGI ID
Datasheet
Strain Description
The gene TNFRSF13C encodes the B cell-activating factor receptor (BAFF-R), also known as BLyS receptor 3 (BR3) or CD268. As a member of the tumor necrosis factor receptor superfamily (TNFRSF), BAFF-R functions as a crucial type III transmembrane signaling protein on lymphocytes. Its expression is predominantly observed on the surface of B cells throughout various stages of their development, from transitional to mature naive and memory populations, underscoring its vital role in peripheral B cell homeostasis [1]. BAFF-R serves as the primary receptor for the cytokine BAFF (TNFSF13B), and their interaction delivers essential survival and maturation signals to B cells, mediated through downstream pathways including the activation of NF-κB and PI3K. Genetic alterations in TNFRSF13C, including point mutations and deletions, or dysregulation of the BAFF-BAFF-R axis, are increasingly recognized for their contribution to immune pathology [2]. Such aberrations are associated with primary immunodeficiencies like common variable immunodeficiency (CVID), characterized by profound defects in antibody production and recurrent infections, as well as a range of autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome, and certain B cell malignancies [2-3]. The critical, non-redundant function of BAFF-R in B cell biology highlights its significance as a key node in adaptive immunity and positions the BAFF-BAFF-R pathway as a compelling target for therapeutic intervention in a spectrum of immune-mediated disorders.
The B6-hBAFFR (hTNFRSF13C) mouse is a humanized model constructed by replacing the sequence of the mouse Tnfrsf13c endogenous extracellular domain in situ with the corresponding extracellular domain 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.
Reference
Schweighoffer E, Tybulewicz VL. BAFF signaling in health and disease. Curr Opin Immunol. 2021 Aug;71:124-131.
Sevdali E, Block Saldana V, Speletas M, Eibel H. BAFF receptor polymorphisms and deficiency in humans. Curr Opin Immunol. 2021 Aug;71:103-110.
Tagami N, Yuda J, Goto Y. Current status of BAFF targeting immunotherapy in B-cell neoplasm. Int J Clin Oncol. 2024 Nov;29(11):1676-1683.
Strain Strategy
The mouse Tnfrsf13c endogenous extracellular domain was replaced with the human TNFRSF13C extracellular domain.
Figure 1. Gene editing strategy of B6-hBAFFR (hTNFRSF13C) Mice.
Application Area
TNFRSF13C-targeted drug screening, development, and evaluation;
Research on the pathological mechanisms and therapeutic approaches of immune-mediated disorders such as common variable immunodeficiency (CVID), systemic lupus erythematosus (SLE), and Sjögren's syndrome;
Research on the pathological mechanisms and therapeutic approaches of certain B cell malignancies.
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