To defend against virus infection, the host activates antiviral machinery. Interferons and IFN-inducible genes (ISGs) are the central components of this response. We detected the upregulation of many IFN-inducible proteins in the cytoplasmic fraction of influenza A virus-infected macrophages (Table S1 ). Interestingly, A. Protein-protein interaction network of all inflammatory proteins identified from intracellular fractions. B. Human macrophages were infected with influenza A virus for 9 h in the presence and absence of AZ11645373 (1 mM), after which the cell culture media was collected and analyzed with IL-18 ELISA. C. Human macrophages were primed with LPS for 18 h, after which the macrophages were infected with influenza A virus for 9 h in the presence and absence of AZ11645373. After this cell culture supernatants were analyzed with IL-1b ELISA. D. Human macrophages were treated with these proteins included three proteins of the IFIT family. It was very recently shown by siRNA approach that interferon-inducible transmembrane proteins (IFITM) restrict an early step of influenza A virus replication in A549 lung epithelial cells [29] . With our proteomics approach we did not detect any inducible expression of IFITM proteins in human macrophages in response to influenza A virus infection. It may be that IFITMs and IFITs function in antiviral response in tissue specific manner and similar to IFITMs, IFIT proteins may be a novel family of antiviral restriction factors that mediate cellular innate immunity to influenza A viruses.