CTAP-III, TG, and NAP-2 are proteolytic truncation products derived from a common precursor (PBP) that is synthesized in megakaryocytes and secreted by activated platelets. NAP-2 is generated by enzymatic processing by leukocytes and is active on neutrophils, affecting chemotaxis, degranulation, adhesion receptor expression, and respiratory burst
via high- and low-affinity interaction with chemokine receptors CXCR2 and CXCR1, respectively. Its precursor CTAP-III also affects metabolic activities in connective tissue cells by as yet unknown mechanisms. In addition to their proinflammatory and reparative functions, these predominantly intravascularly localized chemokines appear to exhibit proinflammatory roles. This is indicated by their modulatory effects, e.g. on megakaryocytopoiesis, on endothelial prostacyclin secretion, on basophil leukocyte histamine release, and even on T cell cytotoxicity.