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Critical role for miR-181a/b-1 in agonist selection of invariant natural killer T cells.

MPG-Autoren

Lyszkiewicz,  Marcin
Max Planck Society;

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Naumann,  Ronald
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

Prinz,  Immo
Max Planck Society;

Krueger,  Andreas
Max Planck Society;

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Zitation

Zietara, N., Lyszkiewicz, M., Witzlau, K., Naumann, R., Hurwitz, R., Langemeier, J., et al. (2013). Critical role for miR-181a/b-1 in agonist selection of invariant natural killer T cells. Proceedings of the National Academy of Sciences of the United States of America, 110(18), 7407-7412.


Zitierlink: http://hdl.handle.net/21.11116/0000-0001-06B0-1
Zusammenfassung
T-cell receptor (TCR) signal strength determines selection and lineage fate at the CD4(+)CD8(+) double-positive stage of intrathymic T-cell development. Members of the miR-181 family constitute the most abundantly expressed microRNA at this stage of T-cell development. Here we show that deletion of miR-181a/b-1 reduced the responsiveness of double-positive thymocytes to TCR signals and virtually abrogated early invariant natural killer T (iNKT) cell development, resulting in a dramatic reduction in iNKT cell numbers in thymus as well as in the periphery. Increased concentrations of agonist ligand rescued iNKT cell development in miR-181a/b-1(-/-) mice. Our results define a critical role of miR-181a/b-1 in early iNKT cell development and show that miR-181a/b-1 sets a TCR signaling threshold for agonist selection.