Interstitial lung disease (ILD) refers to a heterogenous group of diffuse parenchymal lung disorders characterized by varying degrees of inflammation and fibrosis of the pulmonary interstitium. Environmental pollutants such as dust, tobacco and irritant gas are the main causes of ILD. Multiple immune cells were involved in regulating the development of ILD, such as macrophages, lymphocytes, neutrophils, and some subtypes of those cells. Regulatory T cells were reported to adjust the development of ILD, including granulomas and fibrosis. The actual role of these cells in specific ILD are not clear. Besides, a large number of cytokines and chemokines play an important role in the progression from recurrent inflammation to fibrosis in ILD. For example, IL-1beta could accelerate the progress of lung inflammation. IL-10 was considered as regulatory cytokines in lung fibrosis. However, the network of those immune cells and cytokines is still under investigated. Hopefully, the recent development of omics research, including genomics, proteomics and metabonomics, could help researchers to understand the relevant scientific problems more comprehensively.
The goal of this Research Topic is to provide a forum to advance our understanding of the mechanisms underlying the immune regulation in interstitial lung disease, including inflammation, fibrosis as well as granulomas. We welcome Original Research, Review and Mini Review on the sub-topics below:
- The interrelation between immune cells (neutrophils, macrophages, DCs, Treg, Breg, Th17, and NK cells) and effect cells (epithelium, fibroblast, et al.) in Interstitial Lung Disease.
- The network mechanism of immune factors (cytokines, chemokines, et al.).
- Genomics, proteomics and metabonomics studies about interstitial Lung Disease.
Interstitial lung disease (ILD) refers to a heterogenous group of diffuse parenchymal lung disorders characterized by varying degrees of inflammation and fibrosis of the pulmonary interstitium. Environmental pollutants such as dust, tobacco and irritant gas are the main causes of ILD. Multiple immune cells were involved in regulating the development of ILD, such as macrophages, lymphocytes, neutrophils, and some subtypes of those cells. Regulatory T cells were reported to adjust the development of ILD, including granulomas and fibrosis. The actual role of these cells in specific ILD are not clear. Besides, a large number of cytokines and chemokines play an important role in the progression from recurrent inflammation to fibrosis in ILD. For example, IL-1beta could accelerate the progress of lung inflammation. IL-10 was considered as regulatory cytokines in lung fibrosis. However, the network of those immune cells and cytokines is still under investigated. Hopefully, the recent development of omics research, including genomics, proteomics and metabonomics, could help researchers to understand the relevant scientific problems more comprehensively.
The goal of this Research Topic is to provide a forum to advance our understanding of the mechanisms underlying the immune regulation in interstitial lung disease, including inflammation, fibrosis as well as granulomas. We welcome Original Research, Review and Mini Review on the sub-topics below:
- The interrelation between immune cells (neutrophils, macrophages, DCs, Treg, Breg, Th17, and NK cells) and effect cells (epithelium, fibroblast, et al.) in Interstitial Lung Disease.
- The network mechanism of immune factors (cytokines, chemokines, et al.).
- Genomics, proteomics and metabonomics studies about interstitial Lung Disease.
