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

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.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0001-06B0-1 Version Permalink: http://hdl.handle.net/21.11116/0000-0001-06B1-0
Genre: Journal Article

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 Creators:
Zietara, Natalia, Author
Lyszkiewicz, Marcin1, Author
Witzlau, Katrin, Author
Naumann, Ronald2, Author              
Hurwitz, Robert, Author
Langemeier, Jörg, Author
Bohne, Jens, Author
Sandrock, Inga, Author
Ballmaier, Matthias, Author
Weiss, Siegfried, Author
Prinz, Immo1, Author
Krueger, Andreas1, Author
Affiliations:
1Max Planck Society, ou_persistent13              
2Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society, ou_2340692              

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 Abstract: 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.

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 Dates: 2013
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Internal
 Identifiers: eDoc: 688490
Other: 5641
 Degree: -

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Title: Proceedings of the National Academy of Sciences of the United States of America
Source Genre: Journal
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Pages: - Volume / Issue: 110 (18) Sequence Number: - Start / End Page: 7407 - 7412 Identifier: -