English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

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

MPS-Authors

Lyszkiewicz,  Marcin
Max Planck Society;

/persons/resource/persons219480

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

Prinz,  Immo
Max Planck Society;

Krueger,  Andreas
Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: https://hdl.handle.net/21.11116/0000-0001-06B0-1
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.