| First Author | Pan W | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 7096 | PubMed ID | 25963922 |
| Mgi Jnum | J:224880 | Mgi Id | MGI:5689235 |
| Doi | 10.1038/ncomms8096 | Citation | Pan W, et al. (2015) MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis. Nat Commun 6:7096 |
| abstractText | 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. |
