Figures
- FIGURE 1
This schematic view of the morpho-functional unit of the lung (alveolus) depicts the main differences in cellular composition in idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease (SSc-ILD) compared with normal physiological cellular components. Th2: T-helper cell type 2; AEC: alveolar epithelial cell.
- FIGURE 2
Cellular players and molecules in idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease. Cells inside dashed lines are relevant to IPF pathogenesis only. ROS: reactive oxygen species; TGF: transforming growth factor; IL: interleukin; MCP: monocyte chemotactic protein; PDGF: platelet-derived growth factor; ET: endothelin; PMNC: peripheral blood mononuclear cell; EMT: epithelial–mesenchymal transition; CTGF: connective tissue growth factor; Th2: T-helper cell type 2; AEC: alveolar epithelial cell; PMC: pleural mesothelial cell.
Tables
- TABLE 1
Immune cells in idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease (SSc-ILD)
SSc-ILD IPF Macrophage activation IL-4 and IL-13 induce shift to M2 IL-4 and IL-13 induce shift to M2 Macrophage phenotype Scavenger receptor CD163, the IL-1RII decoy receptor, mannose receptors Scavenger receptor CD163, the IL-1RII decoy receptor, mannose receptors Macrophage chemokines IL-10, CCL18, PARC, IL-13, IL-1 receptor antagonist, IL-8, CCL17, CCL2, CCL18, CXCL8, CCL22, S100A9, PDGF and TGF-β IL-10, CCL18, PARC, IL-13, IL-1 receptor antagonist, IL-8, CCL17, CCL2, CCL18, CXCL8, CCL22, S100A9, PDGF and TGF-β T-lymphocyte subpopulations Th2-increased Tregs, Th22, Th17, decreased CXCR3/CXCR4 ratio, increased CD4/CD8 ratio, αvβ3, αvβ5, α4β7 Th2-decreased Tregs, decreased CXCR3/CXCR4 ratio, increased CD4/CD8 ratio, T-lymphocyte chemokines IL-4, IL-5, IL-6, IL-10, IL-13 and IL-22 IL-4, IL-5, IL-10 and IL-13 B-lymphocyte CD19 overexpression, CD19 polymorphism, lymphoid aggregates, elevated BLyS, autoantibody production Elevated BLyS, autoantibody production NK lymphocyte infiltration Yes Yes Mast cell infiltration No Yes Polymorphonuclear cell infiltration Yes Yes Polymorphonuclear cell activity Elastases, oxidative damage Elastases, oxidative damage IL: interleukin; IL-1RII: IL-1 receptor, type II; PARC: pulmonary activation-regulated chemokine; PDGF: platelet-derived growth factor; TGF: transforming growth factor; Th: T-helper cell; Tregs: regulatory T-cells; BLyS: B-lymphocyte stimulator; NK: natural killer.
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- Article
- Abstract
- Abstract
- Introduction
- Myofibroblasts: the effector cells of fibrosis
- Fibroblasts: resident cells, apoptosis and the transition to myofibroblasts
- Fibrocytes: circulating precursors of fibroblasts, collagen-producing monocytes and recruitment to the site of injury
- AECs: pivotal cells in IPF and their role in epithelial–mesenchymal transition
- Endothelial cells: vascular damage, EMT and progenitors
- Pericytes and pleural mesothelial cells: underestimated contributors to mesenchymal transition
- Macrophages: monocyte recruitment, alternative activation and defective efferocytosis
- Lymphocytes: Th2-polarised response and antibody production
- Mast cells: fibrogenesis and lung infiltration
- Polymorphonuclear cells: inflammation and reactive oxygen species injury
- Conclusion
- Footnotes
- References
- Figures & Data
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