Journal
MOLECULAR IMMUNOLOGY
Volume 59, Issue 2, Pages 163-171Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2014.02.004
Keywords
MicroRNA; T cell activation; Interleukin-2; ERK; JNK
Categories
Funding
- Ministry of Science and Technology [2012CB967004, 2012AA020304, 2008BAI51B01, 2012ZX09401012]
- Chinese National Natural Sciences Foundation [81121062]
- Jiangsu Provincial Nature Science Foundation [BE2013630, BZ2012050]
- Bureau of Science and Technology of Changzhou, Jiangsu, China [CM20122003, CZ20120004, WF201207]
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MicroRNAs are small noncoding RNAs that act as posttranscriptional regulators of gene expression. To identify microRNAs involved in T cell activation, we performed a microRNA array profiling with Jurkat cells. We found that microRNA-21 (miR-21), which is upregulated in many tumors by targeting a series of tumor suppressor genes to promote tumor growth, was significantly increased in activated Jurkat cells and primary CD4(+) T lymphocytes compared with that in quiescent counterparts. By using a signaling network building tool, miR-21 was predicted regulates ERK and JNK signaling in activated Jurkat cells. Indeed, miR-21 promotes ERK and JNK signaling in activated T cells. Sproutyl, a direct target of miR-21 that has been shown an inhibitor of ERK and JNK, was also inhibited by forced miR-21 expression in activated T cells. Reciprocally, miR-21 levels were induced by MEK or JNK signaling response to T cell receptor (TCR) engagement. Furthermore, transfection with miR-21 mimic promotes activator protein 1 (AP-1) activity and interleukin-2 (IL-2) expression. These results provide a missing function of miR-21 in TCR-mediated signaling transduction in T lymphocytes, suggesting that miR-21 may augment T cell immune response by a positive feedback mechanism. (c) 2014 Elsevier Ltd. All rights reserved.
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