The human B cell activating factor (BAFF) and APRIL(a proliferation inducing ligand) are both type II molecules belonging to the TNF superfamily (TNFSFL #13b and 13 respectively). They are expressed by non-B cells, and are down regulated by mitogenic stimulation(2). 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(3,4). Ligation of these receptors with recombinant BAFF dramatically increases IgM production by peripheral blood B cells(1). Recently a third receptor for BAFF (BAFF-R) was described(5). BAFF and BAFFR knockout mice have a reduced numbers of mature B cells in the periphery, however TACI and BCMA knockouts do not share this phenotype, suggesting that BAFF-R may the primary receptor for BAFF in mice(8,9,10). Cell surface BAFF can be proteolytically cleaved to form a soluble trimeric molecule(2). Levels of soluble BAFF correspond with levels of autoantibodies in Sjogren's Syndrome(11). Recombinant BAFF(trn)-muCD8 binds to human cell surface TACI/BCMA/BAFFR.