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Steiner, David F.; Thomas, Molly F.; Hu, Joyce K.; Yang, Zhiyong; Babiarz, Joshua E.; Allen, Christopher D.C.; Matloubian, Mehrdad; Blelloch, Robert; Ansel, K. Mark
Immunity (Cambridge, Mass.), 08/2011, Letnik: 35, Številka: 2Journal Article
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. Display omitted ► miRNA -deficient T cells exhibit cell-intrinsic defects in IFN-γ signaling ► Individual miRNAs independently rescue specific defects of miRNA-deficient T cells ► miR-29 negatively regulates IFN-γ production in helper T cells ► IFN-γ repression by miR-29 involves regulation of both T-bet and Eomes
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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