BAFF-R, a Newly Identified TNF Receptor That Specifically Interacts with BAFF
Jeffrey S. Thompson(Biogen (United States)), Sarah A. Bixler(Biogen (United States)), Fang Qian(Biogen (United States)), Kalpit A. Vora(Biogen (United States)), Martin Scott(Biogen (United States)), Teresa G. Cachero(Biogen (United States)), Catherine Hession(Biogen (United States)), Pascal Schneider(Institute for Work and Health), Irene Sizing(Biogen (United States)), Colleen Mullen(Biogen (United States)), Kathy Strauch(Biogen (United States)), Mohammad Zafari(Biogen (United States)), Christopher D. Benjamin(Biogen (United States)), Jürg Tschopp(Institute for Work and Health), Jeffrey L. Browning(Biogen (United States)), Christine Ambrose(Biogen (United States))
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Abstract
B cell homeostasis has been shown to critically depend on BAFF, the B cell activation factor from the tumor necrosis factor (TNF) family. Although BAFF is already known to bind two receptors, BCMA and TACI, we have identified a third receptor for BAFF that we have termed BAFF-R. BAFF-R binding appears to be highly specific for BAFF, suggesting a unique role for this ligand-receptor interaction. Consistent with this, the BAFF-R locus is disrupted in A/WySnJ mice, which display a B cell phenotype qualitatively similar to that of the BAFF-deficient mice. Thus, BAFF-R appears to be the principal receptor for BAFF-mediated mature B cell survival.
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