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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Comparison of soluble decoy IgG fusion proteins of BAFF-R and BCMA as antagonists for BAFF.

BAFF is considered a therapeutic target because dysregulated production of BAFF can induce systemic lupus erythematosus-like phenotype in mice, and elevated levels of BAFF are associated with disease severity in systemic lupus erythematosus and rheumatoid arthritis patients. Fc fusion decoy receptors, BCMA-Fc and BAFF-R-Fc, are therapeutic candidates for blocking BAFF. While studying their interactions with BAFF, we found that BAFF-R-Fc is more effective than BCMA-Fc for blocking BAFF binding to its receptors. We also found that a trimeric BAFF can bind more than one BAFF-R-Fc but only one BCMA-Fc. Moreover, we show that, in contrast to monovalent BAFF-R-Fc, monovalent BCMA does not form stable complexes with BAFF. Differences in their interaction with BAFF predict BAFF-R-Fc would be a better inhibitor. Indeed, we show BAFF-R-Fc is 10-fold more efficacious than BCMA-Fc for blocking BAFF-induced B cell proliferation in vitro and for blocking BAFF-mediated survival of mouse splenic B lymphocytes in vivo.[1]

References

  1. Comparison of soluble decoy IgG fusion proteins of BAFF-R and BCMA as antagonists for BAFF. Pelletier, M., Thompson, J.S., Qian, F., Bixler, S.A., Gong, D., Cachero, T., Gilbride, K., Day, E., Zafari, M., Benjamin, C., Gorelik, L., Whitty, A., Kalled, S.L., Ambrose, C., Hsu, Y.M. J. Biol. Chem. (2003) [Pubmed]
 
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