Pentraxins are a superfamily of acute phase reactants charactarized by a pentameric
structure. The C-reactive protein (CRP) and serum amyloid P-component (SAP) are wellcharactarized short Pentraxins, which are produced in the liver in response to inflammatory mediators. Pentraxin 3 (PTX3), also known as Tumor necrosis factor-Stimulated Gene 14 (TSG-14), is the prototypic long Pentraxin, with a high degree of conservation from mouse to man.
Human PTX3 encodes a 45 kDa secretory glycoprotein with a 162 amino acid N-terminal
extension and a 202 amino acid C-terminal Pentraxin domain. The protein is locally produced and released by a variety of cell types including macrophages, neutrophils, myeloid-derived mesangial cells, synovial cells, smooth muscle cells, alveolar epithelium, and glial cells.
PTX3 is induced in response to either inflammatory cytokines interleukin-1 β (IL-1 β) and tumor necrosis factor α (TNFα) or the selected associated molecular patterns (PAMPs).
PTX3 has a dual role in the regulation of the innate immune response. Via its C-terminal
Pentraxin domain, immobilized PTX3 will bind complement component C1q to induce
classical complement activation. However, fluid-phase PTX3 inhibits classical complement
activation. Furthermore PTX3 participates in the clearance of apoptic cells.
PTX3 is elevated in critically ill patients, with a gradient from systematic inflammatory
resonse syndrome to septic shock, and in several other diseases, such as mycocardial
infarction, rheumatoid arthritis, atherosclerosis, small vessel vasculitis and psoriasis.
Furthermore serum levels of PTX3 are higher in preeclamsia compared with normal
pregancies.
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