| Literature DB >> 20935646 |
Anna-Barbara Stittrich1, Claudia Haftmann, Evridiki Sgouroudis, Anja Andrea Kühl, Ahmed Nabil Hegazy, Isabel Panse, Rene Riedel, Michael Flossdorf, Jun Dong, Franziska Fuhrmann, Gitta Anne Heinz, Zhuo Fang, Na Li, Ute Bissels, Farahnaz Hatam, Angelina Jahn, Ben Hammoud, Mareen Matz, Felix-Michael Schulze, Ria Baumgrass, Andreas Bosio, Hans-Joachim Mollenkopf, Joachim Grün, Andreas Thiel, Wei Chen, Thomas Höfer, Christoph Loddenkemper, Max Löhning, Hyun-Dong Chang, Nikolaus Rajewsky, Andreas Radbruch, Mir-Farzin Mashreghi.
Abstract
After being activated by antigen, helper T lymphocytes switch from a resting state to clonal expansion. This switch requires inactivation of the transcription factor Foxo1, a suppressor of proliferation expressed in resting helper T lymphocytes. In the early antigen-dependent phase of expansion, Foxo1 is inactivated by antigen receptor-mediated post-translational modifications. Here we show that in the late phase of expansion, Foxo1 was no longer post-translationally regulated but was inhibited post-transcriptionally by the interleukin 2 (IL-2)-induced microRNA miR-182. Specific inhibition of miR-182 in helper T lymphocytes limited their population expansion in vitro and in vivo. Our results demonstrate a central role for miR-182 in the physiological regulation of IL-2-driven helper T cell-mediated immune responses and open new therapeutic possibilities.Entities:
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Year: 2010 PMID： 20935646 DOI： 10.1038/ni.1945
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606