The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote TH17 cell-dependent emphysema
作者： Wen Lu , Ran You , Xiaoyi Yuan , Tianshu Yang , Errol L G Samuel
DOI: 10.1038/NI.3292
关键词:
摘要: 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 role microRNA miR-22 in emphysema. We found was upregulated lung myeloid dendritic (mDCs) smokers with and antigen-presenting (APCs) mice exposed to smoke or nanoparticulate carbon black (nCB) mechanism involved transcription factor NF-κB. Mice deficient miR-22, but not wild-type mice, showed attenuated responses failed develop after exposure nCB. further controlled activation APCs AP-1 complexes histone deacetylase HDAC4. Thus, critical regulator both responses.
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