CXCL9-11 were the most highly induced chemokines by influenza viruses as verified at both mRNA and protein levels (Figures 1 and 2) . These three chemokines bind to a common receptor CXCR3, and the importance of CXCR3 signaling has been shown in the pathogenesis of several viruses including influenza [32, [37] [38] [39] . CXCL10 is highly induced in avian flu (H5N1)-infected ferrets, non-human primates, and human cells including alveolar epithelial cells and monocyte-derived macrophages [16] [17] [18] 32, 33, 40] , and has been viewed as a prognostic marker for several viral infections [37, 39, 41, 42] . In mice, the peak level of CXCL11 mRNA coincides with the peak of the viremia [43] , and the CXCL11 protein has been reported to have antiviral activity [44] . In addition, all three CXCR3 ligands can induce epithelial cell chemotaxis and proliferation and perhaps accelerate epithelial wound repair during the resolution of viral infections [45, 46] . The robust induction of CXCL9, 10, and 11 in both AM (Figures 1 and 2) and human alveolar type II cells [34] as well as the distinct CXCL10 response induced by both live and UV-inactivated influenza virus PR/8 and contemporary virus NY/238 (Figure 3 and 4) suggest that this family of proteins likely plays an important role in the human lung alveolar defense against influenza infection, which will require further study.