期刊
NATURE IMMUNOLOGY
卷 16, 期 11, 页码 1185-1194出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3292
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- US National Institutes of Health [R01HL117181, R0IHL110883, AI036211, CA125123, RR024574]
- US Veterans Administration Office of Research and Development [1I01BX002221]
Smoking-related emphysema is a chronic inflammatory disease driven by the T(H)17 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-kappa B. Mice deficient in miR-22, but not wild-type mice, showed attenuated T(H)17 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(H)17 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(H)17 responses.
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