期刊
CELLULAR IMMUNOLOGY
卷 306, 期 -, 页码 35-40出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2016.05.007
关键词
miR-150; AKT3; Bim; CD4(+) T cells; Apoptosis
资金
- National Institutes of Health [CA 94872]
- National Natural Science Foundation of China [08144110]
- Six Talent Peaks Project of Jiangsu Province [2012WS120]
- Natural Science Fund of Higher Education of Jiangsu Province [14KJB320024]
Donor-derived CD4(+) T lymphocytes are the major effector cells directly involved in the development of graft-versus-host disease (GVHD). As a negative regulator of immune cell differentiation and development, microRNA-150 (miR-150) induces immunological tolerance in CD4(+) T cells after transplantation. However, the specific mechanisms have not been fully elucidated. In this study, we demonstrated that miR-150 is capable of not only inhibiting proliferation and activation of CD4(+) T cells but also promoting apoptosis. Mechanistically, miR-150 targets v-akt murine thymoma viral oncogene homolog 3 (AKT3), and subsequently downregulates B-cell lymphoma 2 (Bcl-2) interacting mediator of cell death (BIM). We have also demonstrated that re-expression of AKT3 reversed miR-150-mediated inhibition of CD4(+) T lymphocyte development. Therefore, we conclude that miR-150 negatively regulates CD4(+) T cell function by inhibiting the AKT3/BIM signaling pathway. These findings also suggest that manipulating the levels of miRNA-150 could be a valuable strategy in prevention and/or treatment of acute graft-versus host disease. (C) 2016 Elsevier Inc. All rights reserved.
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