Regulation of miR-181a expression in T cell aging

Zhongde Ye, Guangjin Li, Chulwoo Kim, Bin Hu, Rohit R. Jadhav, Cornelia M. Weyand and Jörg J. Goronzy ()
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Zhongde Ye: Stanford University
Guangjin Li: Stanford University
Chulwoo Kim: Stanford University
Bin Hu: Stanford University
Rohit R. Jadhav: Stanford University
Cornelia M. Weyand: Stanford University
Jörg J. Goronzy: Stanford University

Nature Communications, 2018, vol. 9, issue 1, 1-11

Abstract: Abstract MicroRNAs have emerged as key regulators in T cell development, activation, and differentiation, with miR-181a having a prominent function. By targeting several signaling pathways, miR-181a is an important rheostat controlling T cell receptor (TCR) activation thresholds in thymic selection as well as peripheral T cell responses. A decline in miR-181a expression, due to reduced transcription of pri-miR-181a, accounts for T cell activation defects that occur with older age. Here we examine the transcriptional regulation of miR-181a expression and find a putative pri-miR-181a enhancer around position 198,904,300 on chromosome 1, which is regulated by a transcription factor complex including YY1. The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals. Partial silencing of YY1 in T cells from young individuals reproduces the signaling defects seen in older T cells. In conclusion, YY1 controls TCR signaling by upregulating miR-181a and dampening negative feedback loops mediated by miR-181a targets.

Date: 2018
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DOI: 10.1038/s41467-018-05552-3

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