Experimental and Molecular Pathology

2014

DOI: 10.1016/j.yexmp.2014.07.002

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MICA/B expression in macrophage foam cells infiltrating atherosclerotic plaques

Shunji Ikeshita

¹

,

Yukiko Miyatake

²

,

Noriyuki Otsuka

³

et al.

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Discussion2

Nkg2dls and Myeloid Cells In Disease Settings1

Function Of Nkg2d Ligand Expression By Monocytes and Macroph1

Introduction1

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Cited by 15 publications

(12 citation statements)

References 29 publications

(37 reference statements)

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“…In atherosclerotic plaques , both endothelial cells and macrophages have been reported to express MICA/B ( 15 ). In line with that, exposure of monocyte-derived macrophages to acetylated low-density lipoproteins in vitro led to MICA/B induction ( 168 ). In a mouse model of atherosclerosis, Rae-1 expression was detected on macrophages, not only in plaques but also in the liver, which is affected by metabolic changes associated with disease ( 15 ).…”

Section: Nkg2dls and Myeloid Cells In Disease Settingssupporting

confidence: 56%

The NKG2D/NKG2DL Axis in the Crosstalk Between Lymphoid and Myeloid Cells in Health and Disease

¹

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²

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³

2018

Front. Immunol.

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Natural killer group 2, member D (NKG2D) receptor is a type II transmembrane protein expressed by both innate and adaptive immune cells, including natural killer (NK) cells, CD8+ T cells, invariant NKT cells, γδ T cells, and some CD4+ T cells under certain pathological conditions. NKG2D is an activating NK receptor that induces cytotoxicity and production of cytokines by effector cells and supports their proliferation and survival upon engagement with its ligands. In both innate and T cell populations, NKG2D can costimulate responses induced by other receptors, such as TCR in T cells or NKp46 in NK cells. NKG2D ligands (NKG2DLs) are remarkably diverse. Initially, NKG2DL expression was typically attributed to stressed, infected, or transformed cells, thus signaling “dysregulated-self.” However, many reports indicated their expression under homeostatic conditions, usually in the context of cell activation and/or proliferation. Myeloid cells, including macrophages and dendritic cells (DCs), are among the first cells sensing and responding to pathogens and tissue damage. By secreting a plethora of soluble mediators, by presenting antigens to T cells and by expressing costimulatory molecules, myeloid cells play vital roles in inducing and supporting responses of other immune cells in lymphoid organs and tissues. When activated, both macrophages and DCs upregulate NKG2DLs, thereby enabling them with additional mechanisms for regulating lymphocyte responses. In this review, we will focus on the expression of NKG2D by innate and adaptive lymphocytes, the regulation of NKG2DL expression on myeloid cells, and the contribution of the NKG2D/NKG2DL axis to the crosstalk of myeloid cells with NKG2D-expressing lymphocytes. In addition, we will highlight pathophysiological conditions associated with NKG2D/NKG2DL dysregulation and discuss the putative involvement of the NKG2D/NKG2DL axis in the lymphocyte/myeloid cell crosstalk in these diseases.

“…In atherosclerotic plaques , both endothelial cells and macrophages have been reported to express MICA/B ( 15 ). In line with that, exposure of monocyte-derived macrophages to acetylated low-density lipoproteins in vitro led to MICA/B induction ( 168 ). In a mouse model of atherosclerosis, Rae-1 expression was detected on macrophages, not only in plaques but also in the liver, which is affected by metabolic changes associated with disease ( 15 ).…”

Section: Nkg2dls and Myeloid Cells In Disease Settingssupporting

confidence: 56%

The NKG2D/NKG2DL Axis in the Crosstalk Between Lymphoid and Myeloid Cells in Health and Disease

¹

,

²

,

³

2018

Front. Immunol.

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Natural killer group 2, member D (NKG2D) receptor is a type II transmembrane protein expressed by both innate and adaptive immune cells, including natural killer (NK) cells, CD8+ T cells, invariant NKT cells, γδ T cells, and some CD4+ T cells under certain pathological conditions. NKG2D is an activating NK receptor that induces cytotoxicity and production of cytokines by effector cells and supports their proliferation and survival upon engagement with its ligands. In both innate and T cell populations, NKG2D can costimulate responses induced by other receptors, such as TCR in T cells or NKp46 in NK cells. NKG2D ligands (NKG2DLs) are remarkably diverse. Initially, NKG2DL expression was typically attributed to stressed, infected, or transformed cells, thus signaling “dysregulated-self.” However, many reports indicated their expression under homeostatic conditions, usually in the context of cell activation and/or proliferation. Myeloid cells, including macrophages and dendritic cells (DCs), are among the first cells sensing and responding to pathogens and tissue damage. By secreting a plethora of soluble mediators, by presenting antigens to T cells and by expressing costimulatory molecules, myeloid cells play vital roles in inducing and supporting responses of other immune cells in lymphoid organs and tissues. When activated, both macrophages and DCs upregulate NKG2DLs, thereby enabling them with additional mechanisms for regulating lymphocyte responses. In this review, we will focus on the expression of NKG2D by innate and adaptive lymphocytes, the regulation of NKG2DL expression on myeloid cells, and the contribution of the NKG2D/NKG2DL axis to the crosstalk of myeloid cells with NKG2D-expressing lymphocytes. In addition, we will highlight pathophysiological conditions associated with NKG2D/NKG2DL dysregulation and discuss the putative involvement of the NKG2D/NKG2DL axis in the lymphocyte/myeloid cell crosstalk in these diseases.

“…NKG2D ligand expression and NKG2D ligand-receptor interaction mediated innate immune activation are shown to play important roles in atherosclerotic plaque development 17 26 27 . Sirt6 is an H3K9 and H3K56 deacetylase.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic regulation of NKG2D ligands is involved in exacerbated atherosclerosis development in Sirt6 heterozygous mice

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et al. 2016

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Sirt6 is a member of the class III histone deacetylase family which is associated with aging and longevity. Sirt6 deficient mice show an aging-like phenotype, while male transgenic mice of Sirt6 show increased longevity. Sirt6 acts as a tumor suppressor and deficiency of Sirt6 leads to cardiac hypertrophy and heart failure. Whether Sirt6 is involved in atherosclerosis development, the major cause of cardiovascular diseases, is unknown. We found that the expression of Sirt6 is lower in human atherosclerotic plaques than that in controls. When Sirt6+/−ApoE−/− and ApoE−/− mice are fed with high fat diet for 16 weeks, Sirt6+/−ApoE−/− mice show increased plaque fromation and exhibit feature of plaque instability. Furthermore, Sirt6 downregulation increases expression of NKG2D ligands, which leads to increased cytokine expression. Blocking NKG2D ligand almost completely blocks this effect. Mechanistically, Sirt6 binds to promoters of NKG2D ligand genes and regulates the H3K9 and H3K56 acetylation levels.

“…MICB and ULBP1 were also shown to be upregulated on healthy monocytes from glioblastoma patients in response to tumor-derived lactate dehydrogenase ( 48 ). Additionally, MICA and MICB were observed on foam cells from atherosclerotic lesions as well as human monocyte-derived macrophages treated with acetylated low-density lipoprotein, mimicking atherosclerotic conditions ( 49 ). A study by Ge et al showed that while ULBP1 and MICA were expressed at similar levels by PBMC from children with Kawasaki disease and healthy controls, NKG2D expression by NK cells and CD8 + T cells was decreased in diseased patients, which correlated with increased cytokine production by monocytes ( 50 ).…”

Section: Function Of Nkg2d Ligand Expression By Monocytes and Macrophmentioning

confidence: 99%

More than Decoration: Roles for Natural Killer Group 2 Member D Ligand Expression by Immune Cells

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,

²

2018

Front. Immunol.

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The activating immune receptor natural killer group 2 member D (NKG2D), which is expressed by natural killer cells and T cell subsets, recognizes a number of ligands expressed by “stressed” or damaged cells. NKG2D has been extensively studied for its role in tumor immunosurveillance and antiviral immunity. To date, the majority of studies have focused on NKG2D-mediated killing of target cells expressing NKG2D ligands. However, with a number of reports describing expression of NKG2D ligands by cells that are not generally considered stressed, it is becoming clear that some healthy cells also express NKG2D ligands. Expression of these ligands by cells within the skin, intestinal epithelium, and the immune system suggests other immune functions for NKG2D ligand expression in addition to its canonical role as a “kill me” signal. How NKG2D ligands function in this capacity is just now starting to be unraveled. In this review, we examine the expression of NKG2D ligands by immune cells and discuss current literature describing the effects of this expression on immunity and immune regulation.

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