TNFRSF13C Specific Neutra™ Antibody Products

TNFRSF13C, also more widely known as BAFF receptor (BAFF-R), is a member of the tumor necrosis factor receptor superfamily. It is encoded by the TNFRSF13C gene and expressed on the surface of plasma cells, B cells, and some myeloid cells. The receptor is composed of a cysteine-rich extracellular and transmembrane domain, and an intracellular cytoplasmic tail. BAFF-R binds to the B cell-activating factor (BAFF) and regulates B cell survival, growth, and differentiation. Dysregulation of BAFF-R signaling has been linked to lymphoma and autoimmune illnesses, such as systemic lupus erythematosus (SLE), highlighting its potential as a therapeutic target in these situations.

Its Gene ID: 115650, UniProtKB ID: Q96RJ3, and OMIM ID: 606269.

BAFF/BAFF-R-Mediated B Cell Survival

The BAFF/BAFF-R axis plays a crucial role in promoting B cell survival. Upon binding of BAFF to BAFF-R, several signaling pathways are activated to regulate B cell survival and prevent apoptosis. Activation of the NF-κB pathway increases the expression of anti-apoptotic proteins like Bcl-2 and Bcl-xL, promoting B cell survival. The MAPK pathway regulates cell survival and proliferation through the activation of ERK, JNK, and p38 MAPK. The PI3K/Akt pathway promotes cell survival and proliferation by suppressing apoptosis and activating downstream survival targets including Bad and caspase-9. Additionally, BAFF-R signaling induces the expression of anti-apoptotic factors, including c-FLIP and A1/Bfl-1.

Fig.1 BAFFR-induced intracellular signaling.¹

BAFF/BAFF-R Axis in Lymphomas and Other Diseases

The BAFF/BAFF-R axis has been linked to several illnesses. In lymphomas, dysregulation of BAFF signaling can contribute to B cell malignancies by promoting cell survival, proliferation, and resistance to apoptosis. Overexpression of BAFF or aberrant activation of BAFF-R signaling pathways has been observed in certain types of lymphomas. In autoimmune diseases such as SLE, increased BAFF production and enhanced BAFF-R signaling have been implicated in the pathogenesis. This leads to abnormal B-cell activation, differentiation, and survival, contributing to autoantibody production and immune system dysregulation. Moreover, the BAFF/BAFF-R axis has been associated with other disorders, including rheumatoid arthritis, multiple sclerosis, and atherosclerosis.

Antibodies Targeting BAFF-R

Research on antibodies targeting BAFF-R has shown promising therapeutic effects. Monoclonal antibodies (mAbs) against BAFF-R have demonstrated efficacy in treating SLE by blocking the BAFF/BAFF-R axis, thereby reducing autoreactive B cell survival and plasma cell differentiation. Additionally, studies have investigated the use of BAFF-R mAbs in lymphoma therapy, aiming to disrupt the pro-survival signals mediated by BAFF-R in malignant B cells. Chimeric BAFF-R mAbs have been shown to induce potent ADCC against numerous kinds of human lymphoma and leukemia. Multiple studies have shown that BAFF-R antibodies can also eliminate drug-resistant human B-cell malignancies in vivo and enhance the effectiveness of existing therapeutic drugs for chronic lymphocytic leukemia, which is a promising therapeutic strategy for the treatment of chemoresistance. In general, these anti-BAFF-R antibodies represent a successful novel approach for targeting and treating malignant B-cells and justify continued study.

Creative Biolabs offers thirteen high-quality anti-TNFRSF13C(BAFF-R) antibody products that can be used in several different applications.

REFERENCE

1. Smulski, Cristian R., and Hermann Eibel. "BAFF and BAFF-receptor in B cell selection and survival." Frontiers in immunology 9 (2018): 407701. Distributed under Open Access license CC BY 4.0, without modification.