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Interferon crosstalk at the lung barrier in viral and fungal infection | Infection and Immunity
The pulmonary epithelium maintains a thin barrier that supports efficient alveolar-capillary gas exchange while continuously encountering inhaled particulates, microbes, and toxins (1–3). This barrier favors early containment of pathogens with limited tissue damage before a broader inflammatory response develops (1–3). Within this architecture, epithelial cells sense environmental cues and release mediators that shape local immune responses (1, 4, 5). Along the airway-alveolar axis, epithelial cell identity, transcriptional state, anatomical location, and proximity to immune cells vary, generating distinct responses to the same stimulus (2). Host defense in the lung depends on coordinated signaling between epithelial cells and resident or recruited hematopoietic cells, including macrophages, monocytes, dendritic cells, neutrophils, NK cells, and T cells, which together provide antimicrobial protection (6–9).