期刊
IMMUNITY
卷 35, 期 2, 页码 169-181出版社
CELL PRESS
DOI: 10.1016/j.immuni.2011.07.009
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类别
资金
- Dana Foundation
- Burroughs Wellcome Fund [CABS 1006173]
- UCSF
- UCSF/NIH
- Susan G. Komen Foundation
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.
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