Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic interstitial lung disease with lesions confined to the lungs, preferably in the middle-aged and elderly population, with a characteristic lung histology and/or chest high-resolution CT (HRCT) presentation of common interstitial pneumonia (UIP) with common symptoms: collapse of one side of the chest, telangiectatic breathing, exertional dyspnea, dry cough, pus sputum, and dyspnea. Etiology: immune and inflammatory response (30%): the early stages of PF may produce an anti-specific immune response, the inflammatory response in the lower respiratory tract is the earliest detectable damage to the lung, lymphocytes, macrophages and neutrophils in the interstitium and alveoli are increased, T lymphocytes play a dual role in the regulation of lung injury and disease progression in IPF, T lymphocytes obtained from the alveoli of IPF patients are activated T lymphocytes obtained from the alveoli of IPF patients are activated, express IL-2 receptors and secrete INF-γ. The products secreted by T lymphocytes both inhibit fibroblast proliferation and enhance collagen synthesis in fibroblasts, and in addition, T lymphocytes have a tremendous adjuvant effect on B lymphocytes, which is important for enhancing immune complex production. The generation of specific immune responses within the lung parenchyma is important in influencing the clustering of inflammatory cells in the lung tissue. Selective adhesion molecules, adhesion molecule binding elements and immunoglobulins all play important roles in the interaction between inflammatory cells and endothelial cells, and the firm adhesion of many cells depends on intercellular adhesion molecule-1 (ICAM-1) and leukocyte-acting antigen-1 (LFA-1), and TNF- α induces ICAM-1 expression on the surface of endothelial cells, extravascular leukocytes including LFA-1 and platelet endothelial cell adhesion molecules are expressed at the junction of leukocytes and endothelial cells, fibrinolytic activator of urokinase type (urokinase u-PA) may be a degradation product of protein hydrolases from different tissues during the movement of inflammatory cells from the vasculature to the alveolar lumen, direct migration of inflammatory cells in IPF depend on a variety of chemicals, chemokines including interleukin-1 (IL-1) monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-Ia (MIP-1a), complement component C5a, cytokines (MCP-1, MIP-1a, fibronectin including RGD acting on macrophages, leukotriene B4 (LTB4), IL-8 and C5a for leukocytes, T lymphocytes, alveolar macrophages, endothelial cells, epithelial cells, and fibroblasts are important sources of these cytokines, urokinase receptor (u-PAR, CD87) is an essential chemokine for monocytes and PMN, and U-PAR may affect leukocyte circulation and activate the adhesion function of complement receptor 3. Epithelial cell injury (30%): Epithelial cell injury is a hallmark of IPF, viral infection and inflammatory cellular products (oxygen radicals, protein hydrolases) are mediators of injury, epithelial cell injury allows plasma proteins to leak into the alveolar lumen, the alveolar basal lamina can also be disrupted during injury, and the presence of activated inflammatory cells (lymphocytes, macrophages, PMN) perpetuates the development of alveolar wall injury. Alveolar repair (15%): Successful repair of injured alveoli requires removal of plasma proteins entering the alveolar lumen, replacement of the damaged alveolar wall, and re-stocking of the damaged extracellular matrix. The alveolar exudate formed during the inflammatory response includes many cytokines and mediators such as growth factors (platelet growth factor, transfer growth factor-beta, insulin-like growth factor-I), fibronectin, thromboxane, fibronectin etc., alveolar epithelial cells and macrophages regulate the formation and clearance of fibrin in the alveoli, and there is a reticular fibrin degradation activity in the alveolar lumen due to the presence of μ-PA, however, the fibrin degradation activity in BAL of IPF patients is inhibited due to increased levels of fibrinogen activator and fibrinolytic enzymes such as fibrinogen activation inhibitor-1 (PAI-1), and similarly, the fibrin in the alveolar lumen ligands are also inhibited, and if the alveolar exudate is not cleared, fibroblasts invade, proliferate, and produce new matrix proteins, turning the fibrin-rich exudate into a scar. Fibrosis (10%): Arachidonic acid metabolism also plays an important role in the fibrotic response to IPF. Interleukins have a direct effect on fibroblasts and other mesenchymal cells, stimulating fibroblasts to release chemokines that promote cell proliferation and collagen synthesis. An important feature of alveolar repair is epithelial reformation of the alveolar basement membrane, and to complete this process, type II alveolar epithelial cells proliferate and eventually Basement membrane surface repair and local exudate mechanization, a process that undoubtedly occurs under the influence of keratinocyte growth factor and hepatocyte growth factor, which regulate the proliferation and migration of epithelial cells. During the formation of IPF, epithelial cells are absent, alveoli collapse, and when a large number of alveoli are involved a mass-like scar is formed.