Space-filling model illustrating three molecules of<unk>  (tan/orange) binding a homotrimer of BAFF. . B lymphocytes (B cells), which are part of the normal immune response, are also responsible for the over-aggressive response seen in autoimmune diseases like SLE. B cells develop in the bone marrow and continue to mature peripherally in secondary lymphoid organs and in the gut. When autoimmune B cells attack the body's own tissues, they are normally destroyed by cell suicide (apoptosis). Researchers theorize that SLE is caused when autoimmune B cells proliferate and survival factors protect them from cell suicide. B-cell activating factor (BAFF), also called B-lymphocyte stimulator (BLyS), is required for the development and survival of B cells. In SLE patients, BAFF is overexpressed, which may cause autoimmune B cell proliferation and survival.<unk>  binds to BAFF and prevents it from binding to B cells. Without BAFF, B cells commit suicide and no longer contribute to the autoimmune damage of SLE. BAFF is secreted by a variety of cells: monocytes and macrophages; bone marrow stromal cells; astrocytes in certain glioblastomas; synoviocytes in rheumatoid arthritis; and salivary epithelial cells in Sjögren syndrome. It interacts with three membrane receptors on B lymphocytes: * BAFF-R (BAFF receptor) * BCMA (B cell maturation antigen) * TACI (transmembrane activator and calcium modulator and cyclophylin ligand interactor) When BAFF binds to BAFF-R and BCMA on B cells, levels of Bcl-2, a survival factor, are increased. When all three BAFF receptors are stimulated, levels of NF kappa B, which contributes to cell proliferation and differentiation, are increased in the nucleus. Another B-cell activator similar to BAFF is APRIL (A proliferation-inducing ligand), but APRIL activates only BCMA and TACI, not BAFF-R.<unk>  reduces the number of circulating B cells, but anti-CD20 monoclonal antibodies reduce the number even more. It is possible that<unk>  binds primarily to circulating soluble BAFF and therefore does not induce the antibody-dependent cellular cytotoxicity that could be expected from this IgG1-type antibody..
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