期刊
MUCOSAL IMMUNOLOGY
卷 6, 期 1, 页码 167-176出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2012.60
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资金
- Crohn's and Colitis Foundation of America Research Fellowship Award
- National Institute of Health [R21AI-083609]
Transforming growth factor (TGF)-beta, is an immunosuppressive cytokine that inhibits T-cell activation. We hypothesized that TGF-beta mediates its immunoinhibitory effects by modulation of micro RNA (miRNA)-155 (miR-155). Interleukin (IL)-2 and interferon-gamma are down-regulated by TGF-beta in activated CD4 peripheral blood T cells and lamina propria T cells (LPT), but miR-155 is upregulated ninefold specifically in LPT. Consequently, this study focuses on the role of TGF-beta-enhanced miR-155 on LPT immune responses. TGF-beta induces miR-155 in both freshly isolated and LPT lymphoblasts, whereas other inducible miRNAs are not regulated by TGF-beta. Using MAMI bioinformatics database, we determined that inducible T-cell kinase (itk) is a functional target of miR-155 that exhibits an inverse mRNA response to that of miR-155. To determine experimentally that miR-155 regulates itk, transfection experiments were performed that demonstrated miR-155 overexpression decreased itk and IL-2 mRNA, whereas antagonism of miR-155 restored both mRNAs in activated cells. These findings describe a TGF-beta-dependent function for miR-155 in modulating cytokine and T-cell immune responses in the gut.
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