ArticleImmunology and cell biology2016
Overexpression of Vα14Jα18 TCR promotes development of iNKT cells in the absence of miR-181a/b-1.
Article in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- A high-resolution map of functional miR-181 response elements in the thymus reveals the role of coding sequence targeting and an alternative seed match.Nucleic acids research · 2024Article
- Review
- MicroRNA-181a restricts human γδ T cell differentiation by targeting Map3k2 and Notch2.EMBO reports · 2022Article
- microRNA dynamic expression regulates invariant NKT cells.Cellular and molecular life sciences : CMLS · 2021Review
- MicroRNA miR-181-A Rheostat for TCR Signaling in Thymic Selection and Peripheral T-Cell Function.International journal of molecular sciences · 2020Review
- The Role of MicroRNAs in Development and Function of Regulatory T Cells - Lessons for a Better Understanding of MicroRNA Biology.Frontiers in immunology · 2020Review
- miR-181a/b-1 controls thymic selection of Treg cells and tunes their suppressive capacity.PLoS biology · 2019Article
- T Cell Receptor Expression Timing and Signal Strength in the Functional Differentiation of Invariant Natural Killer T Cells.Frontiers in immunology · 2019Review
- Development of Unconventional T Cells Controlled by MicroRNA.Frontiers in immunology · 2019Review
- Transcriptional and epigenetic regulation of innate-like T lymphocyte development.Current opinion in immunology · 2018Review
- miRNA miR-21 Is Largely Dispensable for Intrathymic T-Cell Development.Frontiers in immunology · 2018Article
- MicroRNA in T-Cell Development and T-Cell Mediated Acute Graft-Versus-Host Disease.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of microRNA miR-181a/b-1 is critical for intrathymic development of invariant natural killer T (iNKT) cells. However, the underlying mechanism has remained a matter of debate. On the one hand, growing evidence suggested that miR-181a/b-1 is instrumental in setting T-cell receptor (TCR) signaling threshold and thus permits agonist selection of iNKT cells through high-affinity TCR ligands. On the other hand, alterations in metabolic fitness mediated by miR-181a/b-1-dependent dysregulation of phosphatase and tensin homolog (Pten) have been proposed to cause the iNKT-cell defect in miR-181-a/b-1-deficient mice. To re-assess the hypothesis that modulation of TCR signal strength is the key mechanism by which miR-181a/b-1 controls the development of iNKT cells, we generated miR-181a/b-1-deficient mice expressing elevated levels of a Vα14Jα18 TCRα chain. In these mice, development of iNKT cells was fully restored. Furthermore, both subset distribution of iNKT cells as well as TCR Vβ repertoire were independent of the presence of miR-181a/b-1 once a Vα14Jα18 TCRα chain was overexpressed. Finally, levels of Pten protein were similar in Vα14Jα18 transgenic mice irrespective of their miR-181a/b-1 status. Collectively, our data support a model in which miR-181 promotes development of iNKT cells primarily by generating a permissive state for agonist selection with alterations in metabolic fitness possibly constituting a secondary effect.
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