Human Pentraxin 3/TSG‑14 Antibody

Pentraxin 3 (PTX3), TSG-14, was initially identified as a TNF-alpha or IL-1 beta inducible gene (1 - 3). It belongs to the pentraxin family, which was named originally for the homo-pentameric structure formed by its members (4). The pentraxin family is divided into two subfamilies: the “short” and the “long” pentraxins with approximate molecular weights of 25 kDa and 50 kDa, respectively. TSG-14 is a member of the long pentraxin subfamily, which also includes the Xenopus laevis XL-PXN1, the guinea pig apexin/p50, the rat neuronal pentraxin I (NPI) and NPR, the human neuronal pentraxin II (NPTX2) and the human neuronal activity-related pentraxin (5). Mature secreted TSG-14 contains a pentaxin-like domain at its carboxy-terminus that shares 23 - 28% amino acid (aa) sequence similarity to C-reactive protein (CRP) and serum amyloid P component (SAP), which belongs to the short pentraxin subfamily. However, the N-terminal sequence of TSG-14 does not share aa sequence homology with any of the “short” pentaxins (3). Unlike CRP and SAP, which forms pentamers only, TSG-14 forms both pentameric and higher ordered oligomers (5). Similarly to CRP and SAP, TSG-14 binds to the complement cascade component C1q (6). However, TSG-14 does not bind to phosphoethanolamine, phosphocholine, or high pyruvate agarose, which are known ligands for CRP and SAP. TSG-14 is a marker of the acute phase response and is highly expressed in advanced atherosclerotic plaques (12). While CRP and SAP are primarily produced in the liver, TSG-14 expression is strongly upregulated by TNF-alpha, IL-1 beta, and bacterial LPS in peripheral fibroblasts, endothelial cells, and macrophages (7). At the amino acid level, human and mouse TSG-14 share 88% aa sequence homology (8). TSG-14 concentration is elevated in the joint fluid of patients with rheumatoid arthritis (RA), indicating that TSG-14 may be a potential mediator of immune response (9). TSG‑14 may also function in the regulation of the uptake and clearance of apoptotic cells by dendritic cells (10). In vivo study showed that TSG-14 transgenic mice are more resistant to sepsis and endotoxemia compared to wild type during the inflammatory injury (11). Increased expression of TSG-14 may enhance the immune response to protect the host from infection.