Immune-mediated
pulmonary diseases are a group of diseases that resulted from immune imbalance initiated by
allergens or of unknown causes. Inflammatory responses without restrictions cause tissue damage and remodeling, which leads to airway hyperactivity, destruction of alveolar architecture, and a resultant loss of lung function. Epigenetic mechanisms have been demonstrated to be involved in
inflammation, autoimmunity, and
cancer. Recent studies have identified that epigenetic changes also regulate molecular pathways in immune-mediated
lung diseases. Aberrant DNA methylation status, dysregulation of histone modifications, as well as altered
microRNAs expression could change transcription activity of genes involved in the development of immune-mediated
pulmonary diseases, which contributes to skewed differentiation of T cells and proliferation and activation of myofibroblasts, leading to overproduction of inflammatory
cytokines and excessive accumulation of extracellular matrix, respectively. Aside from this, epigenetics also explains how environmental exposure influence on gene transcription without genetic changes. It acts as a mediator of the interaction between environmental factors and genetic factors. Identification of the abnormal epigenetic marks in diseases provides novel
biomarkers for prediction and diagnosis and affords novel therapeutic targets for those difficult clinical problems, such as
steroid-resistance and rapidly progressing
fibrosis. In this review, we summarized the latest experimental and translational epigenetic studies in immune-mediated
pulmonary diseases, including
asthma,
idiopathic pulmonary fibrosis,
tuberculosis,
sarcoidosis, and
silicosis.