| First Author | Cho S | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 10 | Pages | 3919-3926 |
| PubMed ID | 28404635 | Mgi Jnum | J:247791 |
| Mgi Id | MGI:5926527 | Doi | 10.4049/jimmunol.1601404 |
| Citation | Cho S, et al. (2017) A Novel miR-24-TCF1 Axis in Modulating Effector T Cell Responses. J Immunol 198(10):3919-3926 |
| abstractText | miR-23 approximately 27 approximately 24 was recently implicated in restricting Th2 immunity, as well as the differentiation and function of other effector T cell lineages. Interestingly, miR-24, unlike other family members, actually promotes Th1 and Th17 responses. In this article, we show that miR-24 drives the production of IFN-gamma and IL-17 in T cells at least in part through targeting TCF1, a transcription factor known for its role in limiting Th1 and Th17 immunity. Surprisingly, whereas TCF1 was previously shown to promote Th2 responses through inducing GATA3, enforced TCF1 expression in miR-24-overexpressing T cells led to further downregulation of IL-4 and GATA3 expression, suggesting miR-24-mediated inhibition of Th2 immunity cannot be attributed to TCF1 repression by miR-24. Together, our data demonstrate a novel miR-24-TCF1 pathway in controlling effector cytokine production by T cells and further suggest miR-24 could function as a key upstream molecule regulating TCF1-mediated immune responses. |
