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- Title
MCPIP1 Down-Regulates IL-2 Expression through an ARE-Independent Pathway.
- Authors
Min Li; Wenqiang Cao; Haifeng Liu; Wei Zhang; Xia Liu; Zhijian Cai; Jing Guo; Xuelian Wang; Zhaoyuan Hui; Hang Zhang; Jianli Wang; Lie Wang
- Abstract
IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 39-untranslated region (39UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-a mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 39UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway.
- Subjects
VIRUSES; ANTIGENS; BACTERIOPHAGES; VACCINE research; EPITOPES
- Publication
PLoS ONE, 2012, Vol 7, Issue 11, p1
- ISSN
1932-6203
- Publication type
Article
- DOI
10.1371/journal.pone.0049841