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Lu, Wen; You, Ran; Yuan, Xiaoyi; Yang, Tianshu; Samuel, Errol L.G; Marcano, Daniela C; Sikkema, William K.A; Tour, James M; Rodriguez, Antony; Kheradmand, Farrah; Corry, David B
Nature immunology, 11/2015Journal Article
Smoking-related emphysema is a chronic inflammatory disease driven by the T.sub.H17 subset of helper T cells through molecular mechanisms that remain obscure. Here we explored the role of the microRNA miR-22 in emphysema. We found that miR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism that involved the transcription factor NF-κB. Mice deficient in miR-22, but not wild-type mice, showed attenuated T.sub.H17 responses and failed to develop emphysema after exposure to smoke or nCB. We further found that miR-22 controlled the activation of APCs and T.sub.H17 responses through the activation of AP-1 transcription factor complexes and the histone deacetylase HDAC4. Thus, miR-22 is a critical regulator of both emphysema and T.sub.H17 responses.
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in: SICRIS
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