Human CD257 (B cell activating factor, BAFF,TALL-1, Blys, THANK) and CD256 (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: CD267 (TACI, transmembrane activator and CAML-interactor) and CD269 (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). A third receptor CD268 (BAFFR) is specific for BAFF has also been 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 BAFFR 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). Clone ANC2H3 binds to recombinant BAFF in EIA and Flow Cytometry and blocks binding of recombinant human CD257(BAFF)trn-muCD8 (catalog #525-020) to receptors on Raji cells in Flow Cytometry.
Isotype: Murine IgG1 Kappa
Immunogen: Recombinant soluble human CD257(BAFF)
Specificity: Antibody ANC2H3 binds to CD257(BAFF) in EIA and blocks binding of recombinant CD257(BAFF)-muCD8 to receptors on Raji cell surface in Flow cytometry.
Functional Application: Antibody ANC2H3 blocks binding of Recombinant CD257(BAFF) to Raji cell surface.
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