TREM-like transcript 2 (TLT2), is expressed on neutrophils, macrophages, and B lymphocytes. Expression of TLT2 is up-regulated on neutrophils and macrophages in response to inflammatory stimuli in vivo and synergizes with agonists that bind to G-protein coupled receptors (GPCR) to potentiate the neutrophil antibacterial and chemotactic response. Administration of anti-TLT2 mAb enhances the acute inflammatory response in vivo that is associated with increased neutrophil recruitment to sites of inflammation. TLT2 ligation in vivo also potentiates chemokine and growth factor production indicating that TLT2 can exert both neutrophil intrinsic and extrinsic effects. The administration of anti-TLT2 mAb alone promotes neutrophil recruitment to the lung and peritoneum, as well as the rapid production of G-CSF, CXCL1 (KC) and CXCL2 (MIP-2). Additionally, the administration of an agent to the circulatory system of an animal can reduce the availability of a TLT2 endogenous ligand to reduce the extent of a neutrophil or macrophage-induced inflammatory response.
