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5. BAFF/BLyS Receptor 3 Binds the B Cell Survival Factor BAFF Ligand through a Discrete Surface Loop and Promotes Processing of NF-κB2

Author

Kayagaki, Nobuhiko, primary, Yan, Minhong, additional, Seshasayee, Dhaya, additional, Wang, Hua, additional, Lee, Wyne, additional, French, Dorothy M., additional, Grewal, Iqbal S., additional, Cochran, Andrea G., additional, Gordon, Nathaniel C., additional, Yin, JianPing, additional, Starovasnik, Melissa A., additional, and Dixit, Vishva M., additional

Published
2002
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7. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete surface loop and promotes processing of NF-kappaB2.

Author

Kayagaki N, Yan M, Seshasayee D, Wang H, Lee W, French DM, Grewal IS, Cochran AG, Gordon NC, Yin J, Starovasnik MA, and Dixit VM

Subjects
Amino Acid Sequence, Animals, Apoptosis, B-Cell Activating Factor, B-Cell Activation Factor Receptor, B-Lymphocytes cytology, Binding Sites, Cell Line, Female, Ligands, Lupus Erythematosus, Systemic immunology, Mice, Mice, Inbred A, Mice, Inbred C57BL, Mice, Inbred NZB, Mice, Knockout, Mice, Mutant Strains, Models, Molecular, Molecular Sequence Data, NF-kappa B p52 Subunit, Protein Processing, Post-Translational, Protein Structure, Tertiary, Receptors, Tumor Necrosis Factor chemistry, Receptors, Tumor Necrosis Factor genetics, Signal Transduction, B-Lymphocytes immunology, B-Lymphocytes metabolism, Membrane Proteins metabolism, NF-kappa B metabolism, Receptors, Tumor Necrosis Factor metabolism, Tumor Necrosis Factor-alpha metabolism
Abstract

The TNF-like ligand BAFF/BLyS is a potent survival factor for B cells. It binds three receptors: TACI, BCMA, and BR3. We show that BR3 signaling promotes processing of the transcription factor NF-kappaB2/p100 to p52. NF-kappaB2/p100 cleavage was abrogated in B cells from A/WySnJ mice possessing a mutant BR3 gene, but not in TACI or BCMA null B cells. Furthermore, wild-type mice injected with BAFF-neutralizing BR3-Fc protein showed reduced basal NF-kappaB2 activation. BR3-Fc treatment of NZB/WF1 mice, which develop a fatal lupus-like syndrome, inhibited NF-kappaB2 processing and attenuated the disease process. Since inhibiting the BR3-BAFF interaction has therapeutic ramifications, the ligand binding interface of BR3 was investigated and found to reside within a 26 residue core domain. When stabilized within a structured beta-hairpin peptide, six of these residues were sufficient to confer binding to BAFF.

Published
2002
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