Baff Binds to the Tumor Necrosis Factor Receptor–Like Molecule B Cell Maturation Antigen and Is Important for Maintaining the Peripheral B Cell Population

Jeffrey S. Thompson(Biogen (United States)), Pascal Schneider(University of Lausanne), Susan L. Kalled(Biogen (United States)), Lichun Wang(Biogen (United States)), Eric A. Lefèvre(Inserm), Teresa G. Cachero(Biogen (United States)), Fabienne Mackay(Garvan Institute of Medical Research), Sarah A. Bixler(Biogen (United States)), Mohammad Zafari(Biogen (United States)), Zhongying Liu(Biogen (United States)), Stephen A. Woodcock(Biogen (United States)), Fang Qian(Biogen (United States)), Marcel Batten(Garvan Institute of Medical Research), Christine Madry(Inserm), Yolande Richard(Inserm), Christopher D. Benjamin(Biogen (United States)), Jeffrey L. Browning(Biogen (United States)), Andréas Tsapis(Inserm), Jürg Tschopp(University of Lausanne), Christine Ambrose(Biogen (United States))
The Journal of Experimental Medicine
July 3, 2000
Cited by 394Open Access
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Abstract

The tumor necrosis factor (TNF) family member B cell activating factor (BAFF) binds B cells and enhances B cell receptor-triggered proliferation. We find that B cell maturation antigen (BCMA), a predicted member of the TNF receptor family expressed primarily in mature B cells, is a receptor for BAFF. Although BCMA was previously localized to the Golgi apparatus, BCMA was found to be expressed on the surface of transfected cells and tonsillar B cells. A soluble form of BCMA, which inhibited the binding of BAFF to a B cell line, induced a dramatic decrease in the number of peripheral B cells when administered in vivo. Moreover, culturing splenic cells in the presence of BAFF increased survival of a percentage of the B cells. These results are consistent with a role for BAFF in maintaining homeostasis of the B cell population.


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