anti-Tumor Necrosis Factor Receptor Superfamily, Member 17 (TNFRSF17) Antibodies

Human Tumor Necrosis Factor Receptor Superfamily, Member 17 (TNFRSF17) interaction partners

1. these data support the further development of anti-BCMA CAR T cells as a potential treatment for not only multiple myeloma (MM)but also some lymphomas

2. Expression patterns of BAFF and its receptor BCMA differ according to lupus nephritis class.

3. High BCMA expression is associated with primary central nervous system lymphoma.

4. soluble BCMA sequesters circulating BAFF, thereby preventing it from performing its signaling to stimulate normal B-cell and plasma cell development, resulting in reduced polyclonal antibody levels in multiple myeloma patients.

5. Studied expression of B-cell maturation antigen (BCMA) in osteoblasts and the toxic effect of chromium on its expression; found BCMA is involved in osteogenesis of osteoblasts; chromium downregulates expression of BCMA in osteoblasts.

6. BCMA has other contributors for ligands binding except DxL motif. The affinity of BCMA for APRIL higher than for BAFF may be caused by the segment outside of the conservative DxL motif. Moreover, the exposition of new binding modes of BCMA2 interacting with APRIL may establish the foundation of designing novel drugs in the future

7. New molecular mechanisms of in vivo Multiple Myeloma (MM) growth and immunosuppression critically dependent on BCMA and APRIL in the Bone marrow microenvironment, further supporting targeting this prominent pathway in MM.

8. We have identified a specific serum protein, BCMA, as a novel independent marker for both monitoring and predicting outcomes for MM patients. We have shown that sBCMA is elevated in MM patients, and can be used to follow their disease status, PFS and OS.

9. The expression levels of serum BAFF and the three receptors (TACI, BCMA and BAFF-R) in non-Hodgkin lymphoma patients were significantly higher than in healthy controls.

10. Decreased BCMA expression on peripheral B cells according to severe disease activity suggests that BCMA plays an important regulating role in B-cell hyperactivity and immune tolerance homeostasis in systemic lupus erythematosus patients

11. results suggest that Akt and JNK pathways are involved in the regulation of B-cell maturation antigen (BCMA)

12. shedding of BCMA by gamma-secretase controls plasma cells in the bone marrow and yields a potential biomarker for B-cell involvement in human autoimmune diseases

13. elevated serum levels in patients with Behcet's disease

14. Data show significant differences in expression of tumour necrosis factor family (BAFF) receptors BAFF-R, BCMA and TACI in patients with and without anti-Jo-1 or anti-Ro52/anti-Ro60 autoantibodies.

15. High BCMA expression is associated with breast cancer.

16. BAFF and APRIL as well as their cognate receptors (BCMA, TACI) correlate with glioma grade. (Meta-analysis)

17. The B cell maturation antigen (BCMA) is a tumor necrosis family receptor member that is predominantly expressed on terminally differentiated B cells and, upon binding to its ligands B cell activator of the TNF family and a proliferation inducing ligand.

18. Activation of B cells through BCMA regulates spinal cord injury-induced autoimmunity via a proliferation-inducing ligand (APRIL) and B-cell-activating factor (BAFF).

19. Data indicate that MAGE3, Survivin and B-cell maturation antigen (BCMA) mRNA-pulsed dendritic cells (DCs) are capable of stimulating tumor-associated antigens (TAA)-specific T-cell responses in multiple myeloma (MM) patients.

20. Data indicate that B-cell maturation antigen (BCMA) is a suitable target for chimeric antigen receptor (CAR)-expressing T cells, and adoptive transfer of anti-BCMA-CAR-expressing T cells is a promising new strategy for treating multiple myeloma.

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 17 (TNFRSF17) interaction partners

1. high affinity antibody blocks the binding of the native ligands APRIL and BAFF to BCMA. This finding is rationalized by the high resolution crystal structure of the Fab fragment in complex with the extracellular domain of BCMA

2. Elimination of B lymphocyte stimulator receptor 3 (BR-3) and BCMA inhibits the development of SLE in NZM mice.

3. we have identified a novel role for BCMA to control excess BAFF production in murine lupus through restraining the accumulation of BAFF-producing neutrophils.

4. Heteromers consisting of one BAFF and two APRIL bind to receptor TACI, BCMA but not to BAFFR.

5. BCMA is dispensable for the development of SLE in NZM mice. BAFF-BCMA interactions contribute to SLE.

6. Study reveals that BCMA works to control B cell homeostasis and self-tolerance in systemic autoimmunity.

7. Blimp-1 is a positive regulator of the expression of BCMA gene in mouse plasma cells.

8. The 5'-flanking sequence from -820 to +145 bp of BCMA is of promoter activity.

9. A vital role of BCMA in bone marrow plasma cell survival.

10. B cell maturation antigen, the receptor for a proliferation-inducing ligand and B cell-activating factor of the TNF family, induces antigen presentation in B cells.

11. Review. APRIL interactions with BCMA likely govern memory B cell populations.

12. Review. Direct BAFF/APRIL signalling in T cells and/or T cell modulation in response to a BAFF-modified B cell compartment may play an important role in inflammation and immunomodulation.