Excessive production of IFN-γ and CXCL10 due to the presence of elevated numbers of CD8+ T cells in lung is thought to contribute to chronic obstructive pulmonary disease (COPD) [15]: it appears that CXCL10 production in CD8+ T cells and bronchiolar epithelium triggers CXCR3 to recruit T lymphocytes, contributing to disease symptoms [16].These previous results in ALI and COPD are consistent with our observations of the joint pro-inflammatory effects of CXCR3 and CXCL10 in our mouse model of acute ALI. The gene discussed is CD8A; the disease is acute respiratory distress syndrome.