| Literature DB >> 11509692 |
J S Thompson1, S A Bixler, F Qian, K Vora, M L Scott, T G Cachero, C Hession, P Schneider, I D Sizing, C Mullen, K Strauch, M Zafari, C D Benjamin, J Tschopp, J L Browning, C Ambrose.
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.Entities:
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Year: 2001 PMID: 11509692 DOI: 10.1126/science.1061965
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728