Mouse B7-H4 Antibody [Biotin]

B7-H4, also known as B7x and B7S1, is a member of the B7 family of immune co-stimulatory proteins (1). Mature B7-H4 is a 50 kDa - 80 kDa glycosylated molecule with a 28 kDa protein core (2). Partial sensitivity to cleavage by PI-PLC suggests a possible GPI linkage of mouse B7-H4 to the cell membrane (3). The 230 amino acid (aa) extracellular region of B7-H4 contains one Ig-like V-set domain and one Ig-like C2-set domain which is followed by a hydrophobic C-terminal region (3 - 5). Within the ECD, mouse B7-H4 shares 90% and 99% aa sequence identity with human and rat B7-H4, respectively. It shares 21% - 29% aa sequence identity with B7-1, B7-2, B7-H1, B7-H2, B7-H3, and PD-L2. B7-H4 expression is induced on mitogen- or LPS-activated B cells, T cells, dendritic cells, monocytes, and macrophages (3, 4) and blocked by GM-CSF or IL-4 (6). It is also expressed on various normal epithelia and upregulated in several carcinomas and renal tubule epithelial cell lesions (2, 6 - 10). B7-H4 is expressed on the surface of macrophages but intracellularly in ovarian and breast cancer cells (2, 6 - 7). It is found in the serum and ascites fluid of cancer patients (11). B7-H4 binds an unidentified ligand on activated T cells which is distinct from BTLA, CD28, CTLA4, ICOS, and PD-1 (3 - 5, 12). Exposure to B7-H4 inhibits antigen-dependent induction of T cell proliferation and activation (3 - 5). Alternatively, B7-H4 expressing renal tubular epithelial cells promote T cell activation (8). Regulatory T cells, IL-6, and IL-10 induce B7-H4 expression on antigen presenting cells which fosters tumor growth by dampening the anti-tumor immune response (6, 13). B7-H4 also promotes the malignant transformation of epithelial cells by protecting them from apoptosis (2). Despite evidence for the involvement of B7-H4 in immune regulation, mice deficient in its expression do not show significant immune deficiencies, suggesting compensation by other molecules in vivo (14).