MiR-214 regulates CD3ζ expression in T cells

T-cell activation requires the T-cell receptor (TCR)-CD3 complex, which integrates and transduces signals. CD3ζ plays a vital role in TCR signalling by mediating T-cell activation. Abnormal CD3ζ expression is a common characteristic of haematological malignancies with T-cell immune dysfunction or au...

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Bibliographic Details
Published in:Central-European journal of immunology 2019-01, Vol.44 (2), p.127-131
Main Authors: Xiao, Yankai, Guo, Lixing, Zhao, Suwen, Huang, Guixuan, Chen, Shaohua, Yang, Lijian, Li, Yangqiu, Li, Bo
Format: Article
Language:English
Subjects:
3' Untranslated regions
Antiretroviral drugs
Autoimmune diseases
cd3
CD3 antigen
Cell activation
Clinical Immunology
Lymphocytes T
MicroRNAs
mir-214
miRNA
Molting
t cell
T cell receptors
Western blotting
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Summary:T-cell activation requires the T-cell receptor (TCR)-CD3 complex, which integrates and transduces signals. CD3ζ plays a vital role in TCR signalling by mediating T-cell activation. Abnormal CD3ζ expression is a common characteristic of haematological malignancies with T-cell immune dysfunction or autoimmune diseases. Targeted regulation of CD3ζ expression by either direct or indirect approaches is important for regulating T-cell activation. In this study, we focused on identifying miRNAs that may regulate CD3ζ expression. Three microRNA target search algorithms (TargetScan, PicTar, and microrna.org) were used to identify hypothetical miRNAs that target CD3ζ in T cells. Of the predicted miRNAs, miR-214 was chosen and validated to determine whether miR-214 directly binds to the CD3ζ 3'-UTR and regulates CD3ζ expression by luciferase reporter assays, real-time PCR, and Western blotting. The results indicate that miR-214 specifically binds the CD3ζ 3'-UTR, and miR-214 mimics remarkably reduce the expression of CD3ζ in MOLT-4 cells. We identify for the first time that miR-214 targets expression in MOLT-4 cells, suggesting that miR-214 might negatively regulate T-cell activation by targeting CD3ζ.
ISSN:1426-3912
1644-4124
DOI:10.5114/ceji.2019.87061