The Role of Immune Cells in the Progression of Idiopathic Pulmonary Fibrosis
DOI:
https://doi.org/10.54097/t84qe494Keywords:
Idiopathic pulmonary fibrosis; immunity; lymphocytes; macrophages; neutrophils.Abstract
Idiopathic Pulmonary Fibrosis (IPF) is a progressive interstitial lung disease of unknown etiology, characterized by the excessive deposition of fibrotic tissue in the lungs. The global incidence of IPF is on the rise, and the disease is associated with a poor prognosis and high mortality rate, with a median survival time of only 2 to 5 years after diagnosis. Pathologically, IPF is most commonly classified into two subtypes: Usual Interstitial Pneumonia (UIP) and Non-Specific Interstitial Pneumonia (NSIP). Current research suggests that injury to alveolar epithelial cells plays a pivotal role in the initiation of IPF. Damaged epithelial cells secrete a variety of cytokines and chemokines, which recruit immune cells, including macrophages, T cells, B cells, and neutrophils, to the lung tissue. These immune cells contribute to local immune dysregulation, leading to further irreversible epithelial injury and the activation of myofibroblasts, which in turn accelerates the progression of fibrosis. This review focuses on the roles of different immune cell populations in the pathogenesis and progression of idiopathic pulmonary fibrosis.
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