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Immunity. 2011 Aug 26;35(2):169-81. doi: 10.1016/j.immuni.2011.07.009. Epub 2011 Aug 4.

MicroRNA-29 regulates T-box transcription factors and interferon-γ production in helper T cells.

Author information

1
Sandler Asthma Basic Research Center and Department of Microbiology & Immunology, University of California, San Francisco, San Francisco, CA 94143, USA.

Abstract

MicroRNA (miRNA)-deficient helper T cells exhibit abnormal IFN-γ 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-γ (IFN-γ) expression. Repression of IFN-γ production by miR-29 involved direct targeting of both T-bet and Eomes, two transcription factors known to induce IFN-γ 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.

PMID:
21820330
PMCID:
PMC3361370
DOI:
10.1016/j.immuni.2011.07.009
[Indexed for MEDLINE]
Free PMC Article

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