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Summary
Braciale, T. J.; Sun, J.; Kim, T. S. Regulating the adaptive immune response to respiratory virus infection. Nature Reviews Immunology 12, 295-305, 2012.

Multiple distinct mechanisms have been postulated to account for the increased susceptibility to bacterial superinfection and bacterial pneumonia following infection with respiratory viruses such as type A influenza viruses. Influenza virus infection induces the production of type I interferons (IFNs), which inhibit the recruitment of circulating neutrophils and macrophages to the lung following bacterial challenge. Type I IFNs also inhibit the differentiation of antibacterial T helper 17 (TH17) cells from naive T cells (TH0 cells) or other TH cell types (such as TH1 and TH2 cells)110 and thereby potentiate host susceptibility to secondary bacterial infection. IFNγ production by influenza virus-specific effector T cells decreases the expression of macrophage receptor with collagenous structure (MARCO) by alveolar macrophages and inhibits the ingestion of bacteria by these cells. Moreover, interleukin-10 (IL-10) production by influenza virus-specific effector T cells may inhibit the ability of innate immune cells, in particular macrophages, to kill bacteria. Finally, the direct interaction and/or infection of innate immune cells — such as macrophages, neutrophils and natural killer (NK) cells — with influenza virus suppresses the ability of these cells to take up and kill bacteria.