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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.

Original publication

DOI

10.1038/ni.1945

Type

Journal article

Journal

Nature immunology

Publication Date

11/2010

Volume

11

Pages

1057 - 1062

Addresses

Deutsches Rheuma-Forschungszentrum Berlin, Berlin, Germany.

Keywords

T-Lymphocytes, Helper-Inducer, Cells, Cultured, Animals, Mice, Inbred BALB C, Mice, Inbred C57BL, Humans, Mice, Arthritis, Disease Models, Animal, MicroRNAs, Interleukin-2, Cell Proliferation