Abstract
Nonhematopoietic cells are emerging as important contributors to many inflammatory diseases, including allergic asthma. Recent advances have led to a deeper understanding of how these cells interact with traditional immune cells, thereby modulating their activities in both homeostasis and disease. In addition to their well-established roles in gas exchange and barrier function, lung epithelial cells express an armament of innate sensors that can be triggered by various inhaled environmental agents, leading to the production of proinflammatory molecules. Advances in cell lineage tracing and single-cell RNA sequencing have expanded our knowledge of rare, but immunologically important nonhematopoietic cell populations. In parallel with these advances, novel reverse genetic approaches are revealing how individual genes in different lung-resident nonhematopoietic cell populations contribute to the initiation and maintenance of asthma. This knowledge is already revealing new pathways that can be selectively targeted to treat distinct forms of asthma.
Footnotes
This work was supported by the Intramural Research Program of the National Institutes of Health, National Institute of Environmental Health Sciences (ZIA ES102025-13).
Abbreviations used in this article:
- AEC
- airway epithelial cell
- AHR
- airway hyperresponsiveness
- AM
- alveolar macrophage
- AT1
- alveolar type 1 cell
- AT2
- alveolar type 2 cell
- BALF
- bronchoalveolar lavage fluid
- BM
- bone marrow
- DC
- dendritic cell
- EC
- epithelial cell
- EV
- extracellular vesicle
- ILC2
- T2 innate lymphoid cell
- MHC-II
- MHC class II
- miRNA
- microRNA
- PNEC
- pulmonary neuroendocrine cell
- scRNA-seq
- single-cell RNA sequencing
- sgRNA
- single-guide RNA
- T2
- type 2
- TSLP
- thymic stromal lymphopoietin.
- Received July 27, 2020.
- Accepted September 28, 2020.
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