Pulmonary fibrosis is a serious lung disease characterized by the destruction of alveolar structures and excessive proliferation of fibrous tissue. The interleukin-17 (IL-17) family consists of six members (IL-17A-17F), which play a crucial role in the occurrence and development of pulmonary fibrosis. The IL-17 family drives pulmonary fibrosis through multiple mechanisms such as pro-inflammatory cytokines, immune cell recruitment, and fibroblast activation. IL-17A is the core molecule, while other members participate in the disease process through synergistic or independent pathways. Targeting the IL-17 signaling axis provides a new strategy for the treatment of pulmonary fibrosis. This article summarizes the effects of IL-17 on pulmonary inflammation response and fibrosis process through literature review, as well as its possible involvement in signal transduction molecular mechanisms, and explores its potential as a therapeutic target, providing theoretical basis for future research aimed at regulating IL-17 expression and function to treat related diseases.
Zhou et al. (Mon,) studied this question.