Fig. 2
From: Role of IL-17 family cytokines in the progression of IPF from inflammation to fibrosis
Main cellular sources and targets of IL-17A and IL-17F in IPF. IL-17A and F can be produced by Th17 cells and other immune cells such as γδ T cells, natural killer cells, macrophages, neutrophils, and non-hematopoietic cells such as epithelial and endothelial cells. IL-17A can contribute to pulmonary fibrosis by EMT, fibroblast proliferation, and differentiation to myofibroblasts. IL-17F stimulates lung inflammation by contributing to the infiltration of neutrophils, macrophages, and lymphocytes as well as promoting the expression of proinflammatory cytokines such as IL-6 and CXC chemokines; however, the role of IL-17F in IPF remains unclear. NK natural killer cells, Th17 T helper cell 17, TNF-α tumor necrosis factor-α, IL-1 interleukin-1, IL-6 interleukin-6, TGF-β transforming growth factor-β, IL-8 interleukin-8, CCL2 C-C motif chemokine 2, CXCL1 C-X-C motif chemokine ligand 1, CXCL5 C-X-C motif chemokine 5, EMT epithelial-mesenchymal transition, α-SMA α-smooth muscle actin, ECM extracellular matrix, IPF idiopathic pulmonary fibrosis