English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Aryl hydrocarbon receptor-mediated induction of the microRNA-132/212 cluster promotes interleukin-17-producing T-helper cell differentiation.

MPS-Authors
/persons/resource/persons14945

Chowdhury,  K.
Facility of Microarray Analyses, MPI for biophysical chemistry, Max Planck Society;

External Resource

http://www.pnas.org/content/110/29/11964.full.pdf+html
(Publisher version)

Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)

1835216.pdf
(Publisher version), 2MB

Supplementary Material (public)

1835216-Suppl.pdf
(Supplementary material), 400KB

Citation

Nakahama, T., Hanieh, H., Nguyen, N. T., Chinen, I., Ripley, B., Millrine, D., et al. (2013). Aryl hydrocarbon receptor-mediated induction of the microRNA-132/212 cluster promotes interleukin-17-producing T-helper cell differentiation. Proceedings of the National Academy of Sciences of the United States of America, 110(29), 11964-11969. doi:10.1073/pnas.1311087110.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0014-4C16-E
Abstract
Aryl hydrocarbon receptor (AHR) plays critical roles in various autoimmune diseases such as multiple sclerosis by controlling in-terleukin- 17 (IL-17)-producing T-helper (T(H)17) and regulatory T cells. Although various transcription factors and cytokines have been identified as key participants in TH17 generation, the role of microRNAs in this process is poorly understood. In this study, we found that expression of the microRNA (miR)-132/212 cluster is up-regulated by AHR activation under T(H)17-inducing, but not regulatory T-inducing conditions. Deficiency of the miR-132/212 cluster prevented the enhancement of T(H)17 differentiation by AHR activation. We also identified B-cell lymphoma 6, a negative regulator of T(H)17 differentiation, as a potential target of the miR-212. Finally, we investigated the roles of the miR-132/212 cluster in experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis. Mice deficient in the miR-132/212 cluster exhibited significantly higher resistance to the development of experimental autoimmune encephalomyelitis and lower frequencies of both T(H)1 and T(H)17 cells in draining lymph nodes. Our findings reveal a unique mechanism of AHR-dependent T(H)17 differentiation that depends on the miR-132/212 cluster.