Table 1.

Preclinical and clinical data of IL-17 family members in pulmonary inflammation and 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	Protective roles in inflammatory response [75, 76]	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

IL-17 interleukin 17, IPF idiopathic pulmonary fibrosis, BLM bleomycin, IL-33 interleukin-33, LPS Lipopolysaccharides, NTHi nontypeable Haemophilus influenzae, PF pulmonary fibrosis, EMT epithelial-mesenchymal transitions, Th17 cells T helper cell 17, IL-13 interleukin-13, ILC2s group II innate lymphoid cells, RA rheumatoid arthritis, ILD interstitial lung disease