期刊
NATURE COMMUNICATIONS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms8096
关键词
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资金
- 973 programme [2014CB541902, 2014CB541901]
- National Natural Science Foundation of China [81230072, 81421001, 81025016, 31370880]
- Key Research Program of the Chinese Academy of Sciences [KSZD-EW-Z-003-3]
- State Key Laboratory of Oncogenes and Related Genes [91-14-05]
- Chinese Ministry of Health [201202008]
- Program of the Shanghai Commission of Science and Technology [12431900703, 12JC1406000, 12ZR1435900]
- Leukemia and Lymphoma Society
- Howard Hughes Medical Institute-The Helen Hay Whitney Foundation
- Shenzhen Foundation of Science and Technology [GJHZ2014041417082192]
Although different autoimmune diseases show discrete clinical features, there are common molecular pathways intimately involved. Here we show that miR-125a is downregulated in peripheral CD4(+) T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells. In miR-125a-deficient mice, the balance appears to shift from immune suppression to inflammation, and results in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE). The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13. Using a chemically synthesized miR-125a analogue, we show potential to re-programme the immune homeostasis in EAE models. These findings point to miR-125a as a critical factor that controls autoimmune diseases by stabilizing Treg-mediated immune homeostasis.
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