Journal
CLINICAL & TRANSLATIONAL IMMUNOLOGY
Volume 8, Issue 6, Pages -Publisher
WILEY
DOI: 10.1002/cti2.1065
Keywords
bacteria; collagen; host defence; macrophage; neutrophil; Toll-like receptors
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Funding
- NHLBI NIH HHS [R35 HL144481] Funding Source: Medline
- NIAID NIH HHS [T32 AI007528, T32 AI007413] Funding Source: Medline
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Lung fibrosis is characterised by the accumulation of extracellular matrix within the lung and is secondary to both known and unknown aetiologies. This accumulation of scar tissue limits gas exchange causing respiratory insufficiency. The pathogenesis of lung fibrosis is poorly understood, but immunologic-based treatments have been largely ineffective. Despite this, accumulating evidence suggests that innate immune cells and receptors play important modulatory roles in the initiation and propagation of the disease. Paradoxically, while innate immune signalling may be important for the pathogenesis of fibrosis, there is also evidence to suggest that innate immune function against pathogens may be impaired, leading to dysregulated and/or impaired host defence. This review summarises the evidence for this pathologic two-way street, highlights new concepts of pathogenesis and recommends future directions for research emphasis.
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