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Molecular and Cellular Pediatrics
Fig. 1 | Molecular and Cellular Pediatrics

Fig. 1

From: Lung epithelial GM-CSF improves host defense function and epithelial repair in influenza virus pneumonia—a new therapeutic strategy?

Fig. 1

GM-CSF-modulated immune response to IV infection. After pulmonary IV infection GM-CSF is released from AEC II, mediated through HGF/c-Met and TGF-α/EGFR signaling. In an autocrine manner, it stimulates epithelial repair, including epithelial proliferation and barrier restoration. Innate and adaptive immunity are activated, resulting in accelerated viral clearance. Via PU.1, GM-CSF improves AM resistance, maturation, ROS production, and phagocytosis capacity, e.g., by the FcγR-mediated opsonophagocytosis. GM-CSF also stimulates activation and proliferation of DCs, especially CD103+ DCs, and T cells and enhances Ag priming and IV-specific CD8+ T cell recruitment. Altogether AEC GM-CSF leads to increased survival and reduced lung injury. AEC alveolar epithelial cells, Ag antigen, AM alveolar macrophage, c-Met hepatocyte growth factor receptor, DC dendritic cell, EGFR epithelial growth factor receptor, FcγR Fcɣ receptor, GM-CSF granulocyte and macrophage colony stimulating factor, HGF hepatocyte growth factor, PU.1 transcription factor PU.1, ROS reactive oxygen species, TGF-α transcriptional growth factor α

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