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Mucosal immunology

A smoke-induced microRNA fires up DCs

Nature Reviews Immunology volume 15, pages 728–729 (2015)Cite this article

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clinical features of smoke-induced emphysema were attenuated in mir-22−/− mice

Initial screens identified a potential pro-inflammatory role for miR-22; the authors proceeded to show that expression of miR-22 is higher in CD1a+ dendritic cells (DCs) from patients with emphysema compared with DCs from control subjects. Similarly, APCs from mice that were exposed to cigarette smoke for 4 months had higher expression of miR-22 compared with APCs from control mice. Wild-type mice exposed to cigarette smoke developed emphysema after 4 months, which was characterized by enlargement of alveolar spaces, increased lung volume and the accumulation of neutrophils, macrophages and TH17 cells in the airways. Strikingly, all of these clinical features of smoke-induced emphysema were attenuated in mir-22−/− mice, suggesting that this microRNA promotes disease development in this model.

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References

  1. Lu, W. et al. The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote TH17 cell-dependent emphysema. Nat. Immunol. 16, 1185–1194 (2015)

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  1. Yvonne Bordon
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Bordon, Y. A smoke-induced microRNA fires up DCs. Nat Rev Immunol 15, 728–729 (2015). https://doi.org/10.1038/nri3935

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