The human B cell activating factor (BAFF) and APRIL (a proliferation inducing ligand) are both type II molecules belonging to the TNF superfamily. They are expressed by non-B cells and are down-regulated by mitogenic stimulation. BAFF and APRIL bind to at least two receptors: TACI (transmembrane activator and CAML-interactor) and BCMA (B cell maturation antigen), both of which are restricted to B cells. Ligation of these receptors with recombinant BAFF dramatically increases IgM production by peripheral blood B cells. Recently a third receptor for BAFF (BAFF-R) was described. BAFF and BAFF-R knockout mice have a reduced number of mature B cells in the periphery. However, TACI and BCMA knockouts do not share this phenotype, suggesting that BAFF-R may be the primary receptor for BAFF in mice. Cell surface BAFF can be cleaved to form a soluble trimeric molecule. Levels of soluble BAFF correspond with levels of autoantibodies in Sjogren’s Syndrome. BCMA-muIg binds to recombinant BAFF-muCD8 and can inhibit binding of this molecule to receptors on Raji cells. BCMA IgG2a Fc, Fusion Protein is a soluble molecule consisting of the extracellular domain (54 amino acids) of human BCMA fused to murine IgG2a Fc (232 amino acids).