Although early induction of IP-10 is helpful in the infiltration of CXCR3+ T lymphocytes and sensing pathogen infection, sustained overexpression of IP-10 in the late stage of endotoxemia resulted in severe lung injury, indicating the importance of IP-10 as an activator that amplifies the proinflammatory response in endotoxemia. This evidence concerns the gene CXCR3 and serum lipopolysaccharide activity.