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Tytuł:
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Hsa-miR-31 Governs T-Cell Homeostasis in HIV Protection via IFN-γ-Stat1-T-Bet Axis.
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Autorzy:
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Zhu L; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.; School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.
Qiu C; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Dai L; Beijing You'an Hospital, Capital Medical University, Beijing, China.
Zhang L; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Feng M; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yang Y; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Qiu C; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zhang A; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Huang J; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Wang Y; Department of AIDS/STD, Shanghai Municipal Center for Disease Control and Prevention, Shanghai, China.
Wan Y; Biomedical Analysis Center, Army Medical University, Chongqing, China.
Zhao C; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Wu H; Beijing You'an Hospital, Capital Medical University, Beijing, China.
Lyu J; School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.
Zhang X; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Xu J; Shanghai Public Health Clinical Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
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Źródło:
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Frontiers in immunology [Front Immunol] 2021 Nov 05; Vol. 12, pp. 771279. Date of Electronic Publication: 2021 Nov 05 (Print Publication: 2021).
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Original Publication: [Lausanne : Frontiers Research Foundation]
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MeSH Terms:
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HIV Infections/*genetics
HIV Infections/*immunology
MicroRNAs/*immunology
T-Lymphocytes/*immunology
Adult ; Biomarkers ; Disease Progression ; Female ; Genetic Predisposition to Disease ; HEK293 Cells ; Homeostasis ; Humans ; Interferon-gamma/immunology ; Male ; Middle Aged ; STAT1 Transcription Factor/immunology ; T-Box Domain Proteins/immunology
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References:
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Contributed Indexing:
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Keywords: CD4+ T cell; HIV-1; STAT1; T-bet; disease progression; miR-31
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Substance Nomenclature:
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0 (Biomarkers)
0 (MIRN31 microRNA, human)
0 (MicroRNAs)
0 (STAT1 Transcription Factor)
0 (STAT1 protein, human)
0 (T-Box Domain Proteins)
0 (T-box transcription factor TBX21)
82115-62-6 (Interferon-gamma)
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Entry Date(s):
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Date Created: 20211122 Date Completed: 20220216 Latest Revision: 20220216
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Update Code:
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20240105
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PubMed Central ID:
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PMC8602903
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DOI:
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10.3389/fimmu.2021.771279
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PMID:
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34804062
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It remains poorly defined whether any human miRNAs play protective roles during HIV infection. Here, focusing on a unique cohort of HIV-infected former blood donors, we identified miR-31 (hsa-miR-31) by comparative miRNA profiling as the only miRNA inversely correlating with disease progression. We further validated this association in two prospective cohort studies. Despite conservation during evolution, hsa-miR-31, unlike its mouse counterpart (mmu-miR-31), was downregulated in human T cell upon activation. Our ex vivo studies showed that inhibiting miR-31 in naïve CD4+ T cells promoted a transcriptional profile with activation signature. Consistent with this skewing effect, miR-31 inhibition led to remarkably increased susceptibility to HIV infection. The suppressive nature of miR-31 in CD4+ T cell activation was pinpointed to its ability to decrease T-bet, the key molecule governing IFN-γ production and activation of CD4+ T cells, by directly targeting the upstream STAT1 transcriptional factor for downregulation, thus blunting Th1 response. Our results implicated miR-31 as a useful biomarker for tracking HIV disease progression and, by demonstrating its importance in tuning the activation of CD4+ T cells, suggested that miR-31 may play critical roles in other physiological contexts where the CD4+ T cell homeostasis needs to be deliberately controlled.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2021 Zhu, Qiu, Dai, Zhang, Feng, Yang, Qiu, Zhang, Huang, Wang, Wan, Zhao, Wu, Lyu, Zhang and Xu.)