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. 2021 Aug 30;2:694514. doi: 10.3389/falgy.2021.694514

Figure 2.

Figure 2

Summary of IL-17 effects on asthma. (A) IL-17 induced neutrophil chemokins production, e.g. CXCL1, CXCL2, CXCL5, GM-CSF, G-CSF, as well as TNF-α, and IFN-γ resulting in increased neutrophil infiltration into the airway; (B) IL-17 induces EMT, increases goblet cell hyperplasia, mucus, and remodeling factor production in epithelial cells; IL-17 stimulates production of TGF-β, ECM deposition as well as transdifferentiation into mesenchymal phenotype in fibroblasts; IL-17 increases mesenchymal cell markers, promotes cell survival, migration, and proliferation, and reduces cell apoptosis, resulting in increased ASM thickness. (C) IL-17 triggers neutrophilic inflammation and AHR in vivo via increasing NF-κB, MEK1, PI3K activity, GR-β and CSF3/G-CSF expression, as well as reduction of HDAC2 activity. These effects might explain the linked between Th17-high inflammation and severe asthma. IL-17, interleukin 17; CXCL-, C-X-C ligand-, GM-CSF, granulocyte-macrophage colony-stimulating factor; G-CSF, granulocyte-colony stimulating factor; TNF-α, tumor necrosis factor α; IFN-γ, interferon γ; EMT, epithelial to mesenchymal transition; TGF-β, transforming growth factor β; ECM, extracellular matrix; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; MEK1, MAP (Mitogen-Activated Protein) Kinase/ERK (Extracellular Signal-Regulated Kinase) Kinase 1; PI3K, phosphoinositide 3-kinase; GR-β, glucocorticoid receptor β; CSF3, colony stimulating factor 3; HDAC2, histone deacetylase 2. Created with BioRender.com.