Inhibition of microRNA-155 ameliorates experimental autoimmune myocarditis by modulating Th17/Treg immune response

Yan, Lianhua; Hu, Fang; Yan, Xiaofei; Wei, Yuzhen; Ma, Wenhan; Ya, Wang; Lü, Shuai; Wang, Zhaohui

doi:10.1007/s00109-016-1414-3

Cited by 73 publications

(50 citation statements)

References 56 publications

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“…Several T-cell intrinsic miRNAs were also found to be dysregulated during the pathogenesis of other autoimmune diseases. The expression of miR-873 43 and miR-326 44 patients with experimental autoimmune myocarditis, 45 miR-200a 46 and miR-210 47 in patients with psoriasis vulgaris, and miR-125a-5p in patients with immune thrombocytopenic purpura 48 were all dramatically increased. The dysregulation of these miRNAs contributes to the disturbed Th17/Treg balance through the promotion of Th17 cell development and/or suppression of Treg cell development.…”

Section: T-cell Intrinsic Mirnasmentioning

confidence: 95%

“…MS is a chronic inflammatory autoimmune disease that damages the central nervous system and has been characterized by demyelinated regions in the white and grey matter of the brain and spinal cord. The chronic inflammatory process in RA indicates that immune regulation in the joint is disturbed and that may be caused by an excessive inflammatory response patients with experimental autoimmune myocarditis, 45 miR-200a 46 and miR-210 47 in patients with psoriasis vulgaris, and miR-125a-5p in patients with immune thrombocytopenic purpura 48 were all dramatically increased. 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.…”

Section: T-cell Intrinsic Mirnasmentioning

confidence: 99%

“…T-bet and Smad7 are two negative regulators of Th17 cell polarization. 28,45 Targets of dysregulated miRNAs in non-T cells STAT1 is a direct target of miR-146a and decreased expression of miR-146a facilitates a pro-inflammatory phenotype of Treg cells because of increased STAT1 activation.…”

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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Section: T-cell Intrinsic Mirnasmentioning

confidence: 95%

Section: T-cell Intrinsic Mirnasmentioning

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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“…23 In miR-155 À/À mice, bone marrow-derived dendritic cells (BMDC) generated fewer pro-inflammatory cytokines, such IL-6 and IL-12 in response to lipopolysaccharide (LPS). [24][25][26] miR-155 overexpression also promoted DC apoptosis, 27 while inhibition of miR-155 induced DC maturation defects, suppressed DC apoptosis, failure to activate T cells but negatively regulated pro-inflammatory cytokine production. 15,27,28 After treatment with the Toll-like receptor (TLR)7 agonist R837, miR-155-transfected plasmacytoid DCs produced less interferon (IFN)-a/b and TNFa.…”

Section: Role Of Mir-155 In Immune Cellsmentioning

confidence: 97%

“…Up‐regulation of miR‐155 in macrophages promoted inflammation and M1 polarization, but inhibited M2 polarization . In miR‐155 −/− mice, bone marrow‐derived dendritic cells (BMDC) generated fewer pro‐inflammatory cytokines, such IL‐6 and IL‐12 in response to lipopolysaccharide (LPS) . miR‐155 overexpression also promoted DC apoptosis, while inhibition of miR‐155 induced DC maturation defects, suppressed DC apoptosis, failure to activate T cells but negatively regulated pro‐inflammatory cytokine production .…”

Section: Role Of Mir‐155 In Immune Cellsmentioning

confidence: 99%

Role of microRNA‐155 in rheumatoid arthritis

Huang

Jia

et al. 2017

Int J of Rheum Dis

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MicroRNAs (miRNAs) are a recently discovered class of post-transcriptional regulators that induce target messenger RNA degradation or translation inhibition. miRNA-155 (miR-155) is an important regulator of immune cells both in humans and mice, by which these cells play critical roles in the pathogenesis of rheumatoid arthritis (RA). Recent findings showed that expression of miR-155 was elevated in RA patients and arthritis models. Moreover, miR-155 overexpression or knockdown performed significantly in the development of arthritis. This review summarizes the recent findings with respect to miR-155 in immune responses and the underlying mechanisms responsible for miR-155-related autoimmune arthritis. Hopefully the information obtained will benefit the development of novel therapeutic strategies.

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The potential role of plasma miR‐155 and miR‐206 as circulatory biomarkers in inflammatory cardiomyopathy

et al. 2021

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Aims Establishing a diagnosis of inflammatory cardiomyopathy (iCMP) by non-invasive means remains challenging despite advances in cardiac magnetic resonance imaging. Previous studies suggested the involvement of microRNAs in the pathogenesis of iCMP. We examined the association of a predefined set of circulatory microRNAs with clinical characteristics of iCMP and evaluated their diagnostic performance in suspected iCMP. Methods and results Eighty-nine patients with clinical suspicion of iCMP were included in the analysis. All patients underwent cardiac catheterization with left ventricular endomyocardial biopsy, echocardiography, and cardiac magnetic resonance imaging applying the Lake Louise criteria (LLC). Plasma levels of miR-21, miR-126, miR-133a, miR-146b, miR-155, and miR-206 were determined using real-time polymerase chain reaction. Based on immunohistological findings on endomyocardial biopsy, iCMP was diagnosed in 67% of study participants (n = 60). Plasma levels of miR-155 and miR-206 were significantly increased in patients with iCMP as compared with patients with dilated cardiomyopathy (P = 0.008 and P = 0.009, respectively). In receiver operating characteristic curve analysis, miR-155 and miR-206 demonstrated superior diagnostic performance for iCMP (0.68 and 0.67, respectively) compared with LLC [area under the curve (AUC) 0.60], Troponin T (AUC 0.51), and N-terminal pro-brain natriuretic peptide (AUC 0.51). While baseline miR-155 and miR-206 plasma levels were predictive for biopsy-proven iCMP (odds ratio = 2.61, 95% confidence interval = 1.28-5.31, P = 0.008 and odds ratio = 2.65, 95% confidence interval = 1.27-5.52, P = 0.009) on univariate logistic regression analysis, the presence of positive LLC, high baseline C-reactive protein, or presence of clinical symptoms and signs of viral infection failed to predict iCMP (P > 0.05, respectively). Conclusions The present data suggest that plasma levels of miR-206 and miR-155 are potential novel biomarkers for confirming the diagnosis of iCMP.

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Inhibition of microRNA-155 ameliorates experimental autoimmune myocarditis by modulating Th17/Treg immune response

Cited by 73 publications

References 56 publications

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

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

Role of microRNA‐155 in rheumatoid arthritis

The potential role of plasma miR‐155 and miR‐206 as circulatory biomarkers in inflammatory cardiomyopathy

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