MicroRNA-590 promotes pathogenic Th17 cell differentiation through targeting Tob1 and is associated with multiple sclerosis

Liu, Qing; Gao, Qing; Li, Zhibao; Mei, Xiaoxue

doi:10.1016/j.bbrc.2017.09.123

Cited by 29 publications

(23 citation statements)

References 25 publications

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“…Investigations of miRNAs have found upregulation of miR-29b ( 36 ), miR-141, miR-200a ( 22 ), miR-155 ( 37 ), miR-223 ( 38 ), miR-326 ( 39 ), let-7e ( 40 ), and miR-448 ( 41 ), and significant downregulation of miR-15a/16-1 ( 42 ) and miR-15b ( 43 ) in CD4 + T cells of MS patients and EAE models. miR-20b ( 44 ) was decreased, while miR-21 ( 45 ) and miR-590 ( 46 ) were increased significantly in Th17 cells compared with Th1, Th2, and inducible Treg cells. In vivo and/or in vitro studies had demonstrated that most of these miRNAs mediated Th17 cell differentiation.…”

Section: Mirnas Mediate Th17 Cell Differentiation In Ms and The Eae Mmentioning

confidence: 95%

Dysregulated MicroRNA Involvement in Multiple Sclerosis by Induction of T Helper 17 Cell Differentiation

et al. 2018

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Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system. Growing evidence has proven that T helper 17 (Th17) cells are one of the regulators of neuroinflammation mechanisms in MS disease. Researchers have demonstrated that some microRNAs (miRNAs) are associated with disease activity and duration, even with different MS patterns. miRNAs regulate CD4+ T cells to differentiate toward various T cell subtypes including Th17 cells. In this review, we discuss the possible mechanisms of miRNAs in MS pathophysiology by regulating CD4+ T cell differentiation into Th17 cells, and potential miRNA targets for current disease-modifying treatments.

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Section: Mirnas Mediate Th17 Cell Differentiation In Ms and The Eae Mmentioning

confidence: 95%

Dysregulated MicroRNA Involvement in Multiple Sclerosis by Induction of T Helper 17 Cell Differentiation

et al. 2018

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“…As of now, most T-cell intrinsic miRNAs that regulate Th17/Treg balance were found during the development and progression of MS and EAE. Although miR-20b, 22 miR-30a, 23 miR-146a, 24 miR-214 25 and miR-26a 26 were down-regulated in CD4 + T cells or Th17 cells during the process of demyelination disease in both patients with MS and EAE mice, the expression of miR-17-92, 27 miR-326, 28 miR-384, 29 miR-181c, 30 miR-21, 31 miR-132/212, 32 miR-155, 33 miR-27a, 25 miR-590, 34 miR-448, 35 miR-141, 36 miR-200a 36 and miR-223 37 was markedly increased. As a consequence, the dysregulation of these miRNAs contributes to the increased Th17 response.…”

Section: T-cell Intrinsic Mirnasmentioning

confidence: 97%

“…Interferon-c mediates the phosphorylation of STAT1, which leads to the expression of T-bet, Smad7 and FasL. 34 Other studies showed that Ets-1, a target of miR-155 and miR-326, may form a protein complex with STAT5, and then inhibit IL-17 expression. In addition, Smad7 inhibits the regulatory function of Treg cells.…”

Section: Targets Of Dysregulated Mirnas In T Cellsmentioning

confidence: 99%

“…60 It has been reported that miR-590 promotes pathogenic Th17 cell differentiation through targeting Tob1. 34 Other studies showed that Ets-1, a target of miR-155 and miR-326, may form a protein complex with STAT5, and then inhibit IL-17 expression. Thereby, miR-155 and miR-326 could promote Th17 differentiation through direct targeting of Ets-1.…”

Section: Targets Of Dysregulated Mirnas In T Cellsmentioning

confidence: 99%

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MicroRNA‐mediated regulation of T helper type 17/regulatory T‐cell balance in autoimmune disease

et al. 2018

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T helper type 17 (Th17) cells and regulatory T (Treg) cells are two distinct T-cell subsets with opposite effects on immune functions. While Th17 cells are a key effector in the immune response and play critical roles in the development of autoimmunity and inflammation, Treg cells orchestrate the overall immune response and maintain peripheral immune tolerance by regulating the activity of the effector T cells. However, the developmental pathways for Th17 and Treg cells are reciprocally interconnected and there is a significant amount of plasticity between them. Disturbed Th17/Treg balance contributes to the development of autoimmune diseases, like experimental autoimmune encephalomyelitis and multiple sclerosis. MicroRNAs (miRNAs) are small non-coding RNA molecules that post-transcriptionally regulate gene expression. Recently, emerging evidence demonstrates that miRNAs play an important role in regulating the pathogenesis of autoimmune diseases through the modulation of Th17/Treg balance. This review will provide an overview of the dysregulated miRNAs and their functions in modulating the Th17/Treg balance in autoimmune diseases.

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“…[10][11][12] Altered expression of miRNAs is closely related to the occurrence of autoimmune diseases, including SLE, [13][14][15][16] rheumatoid arthritis, [17][18][19] and multiple sclerosis. [20][21][22] We previously reported that miR-142-3p specifically targets interleukin-10 (IL-10) and CD84, which are members of the signaling lymphocytic activation molecule (SLAM) family, and that miR-142-5p specifically targets SLAM-associated protein (SAP) by interacting with its 3′-UTR. Inhibition of miR-142-3p/5p in healthy CD4 + T cells led to the increased expression of IL-10, CD84, and SAP as well as T cell overactivation and B cell hyperstimulation.…”

Section: Introductionmentioning

confidence: 99%

BCL-6 suppresses miR-142-3p/5p expression in SLE CD4+ T cells by modulating histone methylation and acetylation of the miR-142 promoter

et al. 2019

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The reduced expression of miR-142-3p/5p in CD4 + T cells of SLE patients caused T cell hyperactivity and B cell hyperstimulation. This study aimed to investigate the mechanisms of regulating miR-142-3p/5p expression in SLE CD4 + T cells. The BCL-6 expression was significantly increased in SLE CD4 + T cells compared with normal controls, and the BCL-6 expression was inversely correlated with miR-142-3p/5p expression. BCL-6 suppresses the expression of miR-142-3p/5p by increasing H3K27me3 level and reducing H3K9/K14ac levels in SLE CD4 + T cells. BCL-6 regulates histone modifications in miR-142 promoter by recruiting EZH2 and HDAC5. Furthermore, we observed significantly decreased CD40L, ICOS, and IL-21 expression levels in SLE CD4 + T cells with BCL-6 interference, and obviously reduced autoantibody IgG production in autologous B cells co-cultured with BCL-6 inhibited SLE CD4 + T cells. Our study found that increased BCL-6 up-regulates H3K27me3 and down-regulates H3K9/14ac at miR-142 promoter in SLE CD4 + T cells. These factors induce a declination in miR-142-3p/5p expression, consequently resulting in CD4 + T cell hyperactivity.

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MicroRNA-590 promotes pathogenic Th17 cell differentiation through targeting Tob1 and is associated with multiple sclerosis

Cited by 29 publications

References 25 publications

Dysregulated MicroRNA Involvement in Multiple Sclerosis by Induction of T Helper 17 Cell Differentiation

Dysregulated MicroRNA Involvement in Multiple Sclerosis by Induction of T Helper 17 Cell Differentiation

MicroRNA‐mediated regulation of T helper type 17/regulatory T‐cell balance in autoimmune disease

BCL-6 suppresses miR-142-3p/5p expression in SLE CD4+ T cells by modulating histone methylation and acetylation of the miR-142 promoter

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