CD317 (BST2, PDCA-1) Monoclonal Antibody (26F8), Alexa Fluor™ 488, eBioscience™, Invitrogen™

Description

• This 26F8 MAb reacts with human CD317 (also known as BST2 and tetherin)
• CD317 is a 30-36-kDa type II transmembrane protein expressed on B cells and bone marrow stromal cells
• Although reports have indicated that CD317 mRNA is detectable in activated T cells, protein expression in freshly isolated primary T cells and macrophages is undetectable
• Moreover, certain T cell lines, such as Jurkat, do not express detectable levels of CD317 protein
• However, CD317 expression can be induced in many cell types (e.g., T and B cells, 293T, and HeLa) by IFNalpha treatment
• CD317 has been associated with pre-B cell growth and the terminal differentiation of plasma B cells
• More recently, this molecule has been reported to prevent HIV-1 virion release from the surface of infected cells, leading to reuptake and degradation of the virus
• This activity is inhibited by the HIV-1 accessory protein Vpu
• CD317 has been identified as the ligand for the ILT7 receptor
• BST2 (CD317, HM1.24 antigen, DAMP-2, tetherin) is an integral membrane protein that is involved in the development and growth of B-cells
• The surface expression of BST2 on fibroblast cell lines facilitated the stromal cell-dependent growth of DW34, a pre-B-cell line
• BST2 is highly expressed during B-cell development, from pro-B precursors to plasma cells, T-cells, monocytes, NK cells and DCs (at protein level), and myeloma cells
• Research studies have shown that BST2 also functions as an inhibitor of retrovirus release from human cells whose activity is antagonized by the HIV-1 accessory protein, Vpu
• While BST2 causes retention of virions on cell surfaces or endocytosis into BST2-positive compartments, its depletion abolished the viral requirement for Vpu for virus release, an activity that may represent a potential therapeutic strategy for the treatment of HIV/AIDS
• Another disease associated with BST2 dysfunction is stomatitis.