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  1. Article ; Online: Decline of miR-124 in myeloid cells promotes regulatory T-cell development in hepatitis C virus infection.

    Ren, Jun P / Wang, Lin / Zhao, Juan / Wang, Ling / Ning, Shun B / El Gazzar, Mohamed / Moorman, Jonathan P / Yao, Zhi Q

    Immunology

    2016  Volume 150, Issue 2, Page(s) 213–220

    Abstract: Myeloid-derived suppressor cells (MDSCs) and microRNAs (miRNAs) contribute to attenuating immune responses during chronic viral infection; however, the precise mechanisms underlying their suppressive activities remain incompletely understood. We have ... ...

    Abstract Myeloid-derived suppressor cells (MDSCs) and microRNAs (miRNAs) contribute to attenuating immune responses during chronic viral infection; however, the precise mechanisms underlying their suppressive activities remain incompletely understood. We have recently shown marked expansion of MDSCs that promote regulatory T (Treg) cell development in patients with chronic hepatitis C virus (HCV) infection. Here we further investigated whether the HCV-induced expansion of MDSCs and Treg cells is regulated by an miRNA-mediated mechanism. The RNA array analysis revealed that six miRNAs were up-regulated and six miRNAs were down-regulated significantly in myeloid cells during HCV infection. Real-time RT-PCR confirmed the down-regulation of miR-124 in MDSCs from HCV patients. Bioinformatic analysis suggested that miR-124 may be involved in the regulation of signal transducer and activator of transcription 3 (STAT-3), which was overexpressed in MDSCs from HCV patients. Notably, silencing of STAT-3 significantly increased the miR-124 expression, whereas reconstituting miR-124 decreased the levels of STAT-3, as well as interleukin-10 and transforming growth factor-β, which were overexpressed in MDCSs, and reduced the frequencies of Foxp3
    MeSH term(s) Cells, Cultured ; Computational Biology ; Down-Regulation ; Forkhead Transcription Factors/metabolism ; Hepacivirus/immunology ; Hepatitis C, Chronic/immunology ; Humans ; Interleukin-10/metabolism ; Lymphocyte Activation/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myeloid-Derived Suppressor Cells/physiology ; Myeloid-Derived Suppressor Cells/virology ; RNA, Small Interfering/genetics ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/virology ; Transforming Growth Factor beta/metabolism
    Chemical Substances FOXP3 protein, human ; Forkhead Transcription Factors ; MIRN124 microRNA, human ; MicroRNAs ; RNA, Small Interfering ; STAT3 Transcription Factor ; STAT3 protein, human ; Transforming Growth Factor beta ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2016-11-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.12680
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Expansion of myeloid-derived suppressor cells promotes differentiation of regulatory T cells in HIV-1+ individuals.

    Wang, Ling / Zhao, Juan / Ren, Jun P / Wu, Xiao Y / Morrison, Zheng D / Elgazzar, Mohamed A / Ning, Shun B / Moorman, Jonathan P / Yao, Zhi Q

    AIDS (London, England)

    2016  Volume 30, Issue 10, Page(s) 1521–1531

    Abstract: Objective: Regulatory T cells (Tregs) contribute to HIV-1 disease progression by impairing antiviral immunity; however, the precise mechanisms responsible for the development of Tregs in the setting of HIV-1 infection are incompletely understood.: ... ...

    Abstract Objective: Regulatory T cells (Tregs) contribute to HIV-1 disease progression by impairing antiviral immunity; however, the precise mechanisms responsible for the development of Tregs in the setting of HIV-1 infection are incompletely understood.
    Design: In this study, we provide evidence that HIV-induced expansion of monocytic myeloid-derived suppressor cells (M-MDSCs) promote the differentiation of Foxp3 Tregs.
    Methods: We measured MDSC induction and cytokine expression by flow cytometry and analyzed their functions by coculturing experiments.
    Results: We observed a dramatic increase in M-MDSC frequencies in the peripheral blood of HIV-1 seropositive (HIV-1) individuals, even in those on antiretroviral therapy with undetectable viremia, when compared with healthy participants. We also observed increases in M-MDSCs after incubating healthy peripheral mononuclear cells (PBMCs) with HIV-1 proteins (gp120 or Tat) or Toll-like receptor 4 ligand lipopolysaccharides in vitro, an effect that could be abrogated in the presence of the phosphorylated signal transducer and activator of transcription 3 inhibitor, STA-21. Functional analyses indicated that M-MDSCs from HIV-1 individuals express higher levels of IL-10, tumor growth factor-β, IL-4 receptor α, p47, programmed death-ligand 1, and phosphorylated signal transducer and activator of transcription 3 - all of which are known mediators of myelopoiesis and immunosuppression. Importantly, incubation of healthy CD4 T cells with MDSCs derived from HIV-1 individuals significantly increased differentiation of Foxp3 Tregs. In addition, depletion of MDSCs from PBMCs of HIV-1 individuals led to a significant reduction of Foxp3 Tregs and increase of IFNγ production by CD4 T effector cells.
    Conclusions: These results suggest that HIV-induced MDSCs promote Treg cell development and inhibit T cell function - a hallmark of many chronic infectious diseases.
    Language English
    Publishing date 2016-06-19
    Publishing country England
    Document type Journal Article
    ZDB-ID 639076-6
    ISSN 1473-5571 ; 0269-9370 ; 1350-2840
    ISSN (online) 1473-5571
    ISSN 0269-9370 ; 1350-2840
    DOI 10.1097/QAD.0000000000001083
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Hepatitis C virus-induced myeloid-derived suppressor cells regulate T-cell differentiation and function via the signal transducer and activator of transcription 3 pathway.

    Ren, Jun P / Zhao, Juan / Dai, Jun / Griffin, Jeddidiah W D / Wang, Ling / Wu, Xiao Y / Morrison, Zheng D / Li, Guang Y / El Gazzar, Mohamed / Ning, Shun B / Moorman, Jonathan P / Yao, Zhi Q

    Immunology

    2016  Volume 148, Issue 4, Page(s) 377–386

    Abstract: T cells play a pivotal role in controlling viral infection; however, the precise mechanisms responsible for regulating T-cell differentiation and function during infections are incompletely understood. In this study, we demonstrated an expansion of ... ...

    Abstract T cells play a pivotal role in controlling viral infection; however, the precise mechanisms responsible for regulating T-cell differentiation and function during infections are incompletely understood. In this study, we demonstrated an expansion of myeloid-derived suppressor cells (MDSCs), in particular the monocytic MDSCs (M-MDSCs; CD14(+) CD33(+) CD11b(+) HLA-DR(-/low) ), in patients with chronic hepatitis C virus (HCV) infection. Notably, HCV-induced M-MDSCs express high levels of phosphorylated signal transducer and activator of transcription 3 (pSTAT3) and interleukin-10 (IL-10) compared with healthy subjects. Blocking STAT3 signalling reduced HCV-mediated M-MDSC expansion and decreased IL-10 expression. Importantly, we observed a significant increase in the numbers of CD4(+) CD25(+) Foxp3(+) regulatory T (Treg) cells following incubation of healthy peripheral blood mononuclear cells (PBMCs) with MDSCs derived from HCV-infected patients or treated with HCV core protein. In addition, depletion of MDSCs from PBMCs led to a significant reduction of Foxp3(+) Treg cells developed during chronic HCV infection. Moreover, depletion of MDSCs from PBMCs significantly increased interferon-γ production by CD4(+) T effector (Teff) cells derived from HCV patients. These results suggest that HCV-induced MDSCs promote Treg cell development and inhibit Teff cell function, suggesting a novel mechanism for T-cell regulation and a new strategy for immunotherapy against human viral diseases.
    MeSH term(s) Cell Proliferation ; Cells, Cultured ; Chronic Disease ; Forkhead Transcription Factors/metabolism ; Hepacivirus/immunology ; Hepatitis C/immunology ; Hepatitis C Antigens/immunology ; Humans ; Interferon-gamma/metabolism ; Interleukin-10/metabolism ; Interleukin-2 Receptor alpha Subunit/metabolism ; Myeloid-Derived Suppressor Cells/physiology ; Myeloid-Derived Suppressor Cells/virology ; STAT3 Transcription Factor/metabolism ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/virology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/virology ; Viral Core Proteins/immunology
    Chemical Substances FOXP3 protein, human ; Forkhead Transcription Factors ; Hepatitis C Antigens ; IL10 protein, human ; Interleukin-2 Receptor alpha Subunit ; STAT3 Transcription Factor ; STAT3 protein, human ; Viral Core Proteins ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.12616
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.181: Show issues Location:
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  4. Article ; Online: Protection of CD4+ T cells from hepatitis C virus infection-associated senescence via ΔNp63-miR-181a-Sirt1 pathway.

    Zhou, Yun / Li, Guang Y / Ren, Jun P / Wang, Ling / Zhao, Juan / Ning, Shun B / Zhang, Ying / Lian, Jian Q / Huang, Chang X / Jia, Zhan S / Moorman, Jonathan P / Yao, Zhi Q

    Journal of leukocyte biology

    2016  Volume 100, Issue 5, Page(s) 1201–1211

    Abstract: T cell dysfunction has a crucial role in establishing and maintaining viral persistence. We have previously shown a decline in miR-181a, which regulates ... ...

    Abstract T cell dysfunction has a crucial role in establishing and maintaining viral persistence. We have previously shown a decline in miR-181a, which regulates CD4
    MeSH term(s) Adult ; Aged ; CD4-Positive T-Lymphocytes/immunology ; Case-Control Studies ; Cellular Senescence ; Female ; Genes, Reporter ; Hepatitis C, Chronic/immunology ; Humans ; Interleukin-2/biosynthesis ; Interleukin-2/genetics ; Male ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; MicroRNAs/physiology ; Middle Aged ; Signal Transduction/immunology ; Sirtuin 1/biosynthesis ; Sirtuin 1/genetics ; Sirtuin 1/physiology ; Telomere Shortening ; Transcription Factors/biosynthesis ; Transcription Factors/genetics ; Transcription Factors/physiology ; Transfection ; Tumor Suppressor Proteins/biosynthesis ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/physiology ; Up-Regulation
    Chemical Substances Interleukin-2 ; MIrn181 microRNA, human ; MicroRNAs ; TP63 protein, human ; Transcription Factors ; Tumor Suppressor Proteins ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
    Language English
    Publishing date 2016-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.5A0316-119RR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: Show issues Location:
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