Human B7-H4 Antibody Summary
Accession # Q727D3
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of B7‑H4 in HEK293 Human Cell Line Transfected with Human B7-H4 and eGFP by Flow Cytometry. HEK293 human embryonic kidney cell line transfected with either (A) human B7-H4 or (B) irrelevant transfectants and eGFP were stained with Mouse Anti-Human B7‑H4 Monoclonal Antibody (Catalog # MAB6576) followed by Allophycocyanin-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # F0101B).
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
B7-H4, also known as VTCN1, B7x and B7S1, is a 50‑80 kDa glycosylated member of the BTN/MOG family of immunomodulatory protein (1, 2). Mature human B7-H4 consists of a 235 amino acid (aa) extracellular domain (ECD) with one Ig-like V-set domain and one Ig-like C2-set domain, a 21 aa transmembrane segment, and a 2 aa cytoplasmic tail (3-5). Within the ECD, human B7-H4 shares 90% aa sequence identity with mouse and rat B7-H4. It shares 22%-28% aa sequence identity with human B7-1, B7-2, B7-H1, B7-H2, B7-H3, and PD‑L2. Alternate splicing of human B7-H4 generates an additional isoform that lacks the first Ig-like domain. B7-H4 is expressed on the surface of activated lymphocytes, macrophages, monocytes, dendritic cells, epithelial cells, and bone marrow-derived mesenchymal stem cells
(4-8). Following binding to activated T cells, B7-H4 serves as a co‑inhibitor of the T cell response. This is accomplished by reverse signaling that can induce either cell cycle arrest, or apoptosis in B7-H4 expressing cells (3-5, 9, 10). B7‑H4 is up‑regulated in several carcinomas in correlation with tumor progression and metastasis (2, 7, 11, 12). A soluble form of B7-H4 is elevated in the serum of ovarian cancer, renal cell carcinoma, and rheumatoid arthritis patients, also in correlation with advanced disease status (13-15). Soluble B7‑H4 functions as a decoy molecule that blocks the inhibitory influence of B7‑H4 on immune activation (15). 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 (16).
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Cells were transfected with hB7-H4 or a negative control. Cells were stained with MAB6576 using a 1/500 dilution and binding was detected with an anti-mouse 594 secondary antibody.