Hypersensitive pneumonitis: etiopathogenetic mechanisms of disease progression

Abstract

Hypersensitivity pneumonitis is a chronic immune-mediated inflammatory lung disease that develops as a result of repeated exposure to inhaled organic or inorganic antigens. This article presents an analysis of current data on etiological factors, pathogenetic mechanisms, and regional features of disease distribution. The key elements of immunopathogenesis are discussed, including the role of T-cell-mediated immune responses, cytokine regulation, and fibrogenesis. The significance of genetic factors, such as HLA polymorphisms and telomere shortening, which determine individual susceptibility and disease severity, is highlighted. Particular attention is given to the study of potential biomarkers reflecting the activity of inflammation and fibrotic remodeling. The article emphasizes the challenges of late diagnosis and the difficulties in identifying causative antigens. Local factors, including climatic and occupational exposures, influence the risk of sensitization and disease development. A comprehensive understanding of the etiology, pathogenesis, and molecular mechanisms of hypersensitivity pneumonitis contributes to improving approaches for early detection, differential diagnosis, and prognostic assessment. In addition, the review summarizes the results of recent studies demonstrating the overlap between fibrotic hypersensitivity pneumonitis and idiopathic pulmonary fibrosis, particularly in molecular and histopathological patterns. These findings underline the need for timely recognition of fibrotic transformation and the integration of molecular biomarkers into clinical practice. Given the lack of large-scale national studies, further research focusing on local environmental and occupational factors in Kazakhstan is crucial for clarifying regional patterns of antigen exposure and disease progression.