| First Author | Steiner DF | Year | 2011 |
| Journal | Immunity | Volume | 35 |
| Issue | 2 | Pages | 169-81 |
| PubMed ID | 21820330 | Mgi Jnum | J:175847 |
| Mgi Id | MGI:5287530 | Doi | 10.1016/j.immuni.2011.07.009 |
| Citation | Steiner DF, et al. (2011) MicroRNA-29 Regulates T-Box Transcription Factors and Interferon-gamma Production in Helper T Cells. Immunity 35(2):169-81 |
| abstractText | MicroRNA (miRNA)-deficient helper T cells exhibit abnormal IFN-gamma production and decreased proliferation. However, the contributions of individual miRNAs to this phenotype remain poorly understood. We conducted a screen for miRNA function in primary T cells and identified individual miRNAs that rescue the defects associated with miRNA deficiency. Multiple members of the miR-17 and miR-92 families enhanced miRNA-deficient T cell proliferation whereas miR-29 largely corrected their aberrant interferon-gamma (IFN-gamma) expression. Repression of IFN-gamma production by miR-29 involved direct targeting of both T-bet and Eomes, two transcription factors known to induce IFN-gamma production. Although not usually expressed at functionally relevant amounts in helper T cells, Eomes was abundant in miRNA-deficient cells and was upregulated after miR-29 inhibition in wild-type cells. These results demonstrate that miR-29 regulates helper T cell differentiation by repressing multiple target genes, including at least two that are independently capable of inducing the T helper 1 (Th1) cell gene expression program. |
