LP17, a synthetic peptide mimicking highly conserved extracellular domain of TREM-1, decreased the cytokine production in human monocytes and protected septic animals from hyper-responsiveness and death.[11,29] A chimeric protein TREM-1/IgG1 (equivalent to the extracellular domain of TREM-1) blocked TREM-1 activation during endotoxemia and peritonitis in C57BL/6 mice.[13]. The gene discussed is TREM1; the disease is serum lipopolysaccharide activity.