Table 1 Preclinical and clinical data of IL-17 family members in pulmonary inflammation and fibrosis
From: Role of IL-17 family cytokines in the progression of IPF from inflammation to fibrosis
IL-17 family member | Expression changes in inflammatory lung | Preclinical role in PF | Clinical role in PF |
|---|---|---|---|
IL-17A | Elevated in BLM, IL-33 and LPS-induced lung inflammation [36, 44] | Contributing to fibrosis by promoting proinflammatory cytokines [39, 43]; triggering neutrophilia [44]; promoting EMT [46], accelerating fibroblasts proliferation, differentiation [46, 49] | Elevated in: lung of RA-ILD patients [35];airways of cystic fibrosis patients [34] |
IL-17B | Expression of IL-17B was induced by dysregulated microbiota [63] | Elevated in BLM-induced PF mouse model by regulating Th17-cell-promoting genes and neutrophil-recruiting genes [63] | No data |
IL-17C | IL-17C contributes to NTHi-induced inflammation and lung damage [74] | Remains limited | No data |
IL-17D | Remains limited | Remains limited | No data |
IL-17E | Drove lung fibrosis by mediating EMT; recruiting and activating lung fibroblasts [80]; promotes IL-13 from ILC2s; triggering collagen deposition [81] | Elevated in lung of IPF patients [80] | |
IL-17F | Recruitment of neutrophils, macrophages, lymphocytes; promotes inflammatory cytokines [52, 55] | No direct evidence for the progression of IPF | Â |