Cutting Edge: MicroRNA-181 Promotes Human NK Cell Development by Regulating Notch Signaling

Cichocki, Frank; Felices, Martin; McCullar, Valarie; Presnell, Steven R.; Al‐Attar, Ahmad; Lütz, Cornelius; Miller, Jeffrey S.

doi:10.4049/jimmunol.1100835

Cited by 153 publications

(137 citation statements)

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“…Recent advances have demonstrated that miRNAs are crucial in NK cell biology [50] . For instance, miR150 and miR181 regulate NK cell development [51,52] . Mice lacking miR150…”

Section: Mirnas and Nk Cellsmentioning

confidence: 99%

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miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Zhang

2016

WJG

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Inflammatory bowel disease (IBD) is characterized by chronic relapsing inflammatory disorders of the gastrointestinal tract, and includes two major phenotypes: ulcerative colitis and Crohn's disease. The pathogenesis of IBD is not fully understood as of yet. It is believed that IBD results from complicated interactions between environmental factors, genetic predisposition, and immune disorders. miRNAs are a class of small non-coding RNAs that can regulate gene expression by targeting the 3′-untranslated region of specific mRNAs for degradation or translational inhibition. miRNAs are considered to play crucial regulatory roles in many biologic processes, such as immune cellular differentiation, proliferation, and apoptosis, and maintenance of immune homeostasis. Recently, aberrant expression of miRNAs was revealed to play an important role in autoimmune diseases, including IBD. In this review, we discuss the current understanding of how miRNAs regulate autoimmunity and inflammation by affecting the differentiation, maturation, and function of various immune cells. In particular, we focus on describing specific miRNA expression profiles in tissues and peripheral blood that may be associated with the pathogenesis of IBD. In addition, we summarize the opportunities for utilizing miRNAs as new biomarkers and as potential therapeutic targets in IBD.

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“…Recent advances have demonstrated that miRNAs are crucial in NK cell biology [50] . For instance, miR150 and miR181 regulate NK cell development [51,52] . Mice lacking miR150…”

Section: Mirnas and Nk Cellsmentioning

confidence: 99%

“…miR181 promotes NK cell development by targeting Nemolike kinase, which is a inhibitor of Notch signaling [52] .…”

Section: Mirnas and Nk Cellsmentioning

confidence: 99%

miRNAs as new molecular insights into inflammatory bowel disease: Crucial regulators in autoimmunity and inflammation

Zhang

2016

WJG

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“…6 Three research groups have identified the top 20 miRNAs expressed in mouse and human NK cells using next-generation sequencing. [7][8][9] Thus far, the miRNAs that have been identified as ones involved in NK cell development are miR-150 and miR-181a/b, which target c-Myb 10 and NEMO-like kinase 11 , respectively. Moreover, miRNAs have been shown to regulate NK cell functions.…”

Section: Introductionmentioning

confidence: 99%

miR-146a negatively regulates NK cell functions via STAT1 signaling

Han

Hou

et al. 2016

Cell Mol Immunol

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It is known that natural killer (NK) cell function is downregulated in chronic hepatitis B (CHB)-infected patients and in hepatic carcinoma (HCC) patients, but the mechanisms underlying this functional downregulation are largely unclear. In this study, microRNA (miR)-146a expression increased in NK cells from CHB and HCC patients compared with NK cells from healthy donors, and miR-146a levels were negatively correlated to NK cell functions. Overexpression of miR-146a reduced NK cell-mediated cytotoxicity and the production of interferon (IFN)-γ and tumor necrosis factor-α, which were reversed upon inhibition of miR-146a. In NK cells, miR-146a expression was induced by interleukin (IL)-10 and transforming growth factor-β, but reduced after treatment with interleukin-12, IFN-α and IFN-β. We further revealed that miR-146a regulated NK cell functions by targeting STAT1. Taken together, upregulated miR-146a expression, at least partially, attributes to NK cell dysfunction in CHB and HCC patients. Therefore, miR-146a may become a therapeutic target with great potential to ameliorate NK cell functions in liver disease.

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“…MicroRNA-23b is capable of inducing tolerogenic properties of dendritic cells in vitro through the inhibition of the Notch1 and NF-κB signalling pathways [80]. MicroRNA-181 promotes natural killer (NK) cell development by regulating Notch signaling [81]. MiR-124a mediates stroke-induced neurogenesis by targeting the JAG-Notch signaling pathway [82].…”

Section: Notch Signaling Pathwaymentioning

confidence: 99%