2016
DOI: 10.1038/icb.2016.40
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Overexpression of Vα14Jα18 TCR promotes development of iNKT cells in the absence of miR‐181a/b‐1

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 phosphata… Show more

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Cited by 22 publications
(24 citation statements)
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“…This interpretation is consistent with the hypothesis that miR‐181a serves as a rheostat for TCR signaling during thymic selection . In addition, this finding parallels the consequences of miR‐181a/b‐1‐deficiency on development of iNKT cells . Furthermore, these data show that late‐stage proliferation in the thymus is unable to compensate for ineffective generation of both MAIT and iNKT cells.…”
Section: Discussionsupporting
confidence: 88%
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“…This interpretation is consistent with the hypothesis that miR‐181a serves as a rheostat for TCR signaling during thymic selection . In addition, this finding parallels the consequences of miR‐181a/b‐1‐deficiency on development of iNKT cells . Furthermore, these data show that late‐stage proliferation in the thymus is unable to compensate for ineffective generation of both MAIT and iNKT cells.…”
Section: Discussionsupporting
confidence: 88%
“…This distribution was not markedly altered upon ectopic expression of the invariant Vα19Jα33 TCRα chain. However, phenotypic differences based on surface markers were also observed in iNKT cells from Vα14 transgenic mice . Therefore, we also analyzed expression of PLZF.…”
Section: Resultsmentioning
confidence: 99%
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“…Lastly, the authors showed that the defect in MAIT cell development in the absence of miR‐181a/b‐1 could be partially overcome by forced expression of a transgenic MAIT TCR‐α chain (Vα19Jα33) . This is similar to how transgenic expression of the semi‐invariant NKT TCRα chain (Vα14Jα18) restores NKT development in miR‐181a/b‐1 −/− mice and suggests a similar mechanism by which miR‐181a/b‐1 regulate both cell types. It is possible that this simply reflects a slightly higher level of transgenic TCR expression that can overcome a signaling defect in the absence of miR‐181a/b‐1, but regardless, this restoration in MAIT cell numbers was incomplete.…”
mentioning
confidence: 74%