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  1. Article ; Online: Effect of NKG2D ligand expression on host immune responses.

    Champsaur, Marine / Lanier, Lewis L

    Immunological reviews

    2010  Volume 235, Issue 1, Page(s) 267–285

    Abstract: ... I molecules. There is increasing evidence that ligand expression can result in both immune activation (tumor ... In this review, we describe this family of NKG2D ligands and the various mechanisms that control their expression ... in stressed and normal cells. We also discuss the host response to both membrane-bound and secreted NKG2D ...

    Abstract Natural killer group 2, member D (NKG2D) is an activating receptor present on the surface of natural killer (NK) cells, some NKT cells, CD8(+) cytotoxic T cells, gammadelta T cells, and under certain conditions CD4(+) T cells. Present in both humans and mice, this highly conserved receptor binds to a surprisingly diverse family of ligands that are distant relatives of major histocompatibility complex class I molecules. There is increasing evidence that ligand expression can result in both immune activation (tumor clearance, viral immunity, autoimmunity, and transplantation) and immune silencing (tumor evasion). In this review, we describe this family of NKG2D ligands and the various mechanisms that control their expression in stressed and normal cells. We also discuss the host response to both membrane-bound and secreted NKG2D ligands and summarize the models proposed to explain the consequences of this differential expression.
    MeSH term(s) Animals ; Autoimmunity ; Cytotoxicity, Immunologic ; GPI-Linked Proteins ; Histocompatibility Antigens Class I/immunology ; Humans ; Intercellular Signaling Peptides and Proteins/immunology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/virology ; Ligands ; Mice ; NK Cell Lectin-Like Receptor Subfamily K/immunology ; Neoplasms/immunology ; Signal Transduction ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/virology ; Tumor Escape ; Viruses/immunology ; Viruses/pathogenicity
    Chemical Substances GPI-Linked Proteins ; Histocompatibility Antigens Class I ; Intercellular Signaling Peptides and Proteins ; Ligands ; NK Cell Lectin-Like Receptor Subfamily K ; ULBP2 protein, human
    Language English
    Publishing date 2010-06-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/j.0105-2896.2010.00893.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Effect of NKG2D ligand expression on host immune responses

    Champsaur, Marine / Lanier, Lewis L

    Immunological reviews. 2010 May, v. 235, no. 1

    2010  

    Abstract: ... I molecules. There is increasing evidence that ligand expression can result in both immune activation (tumor ... In this review, we describe this family of NKG2D ligands and the various mechanisms that control their expression ... in stressed and normal cells. We also discuss the host response to both membrane-bound and secreted NKG2D ...

    Abstract Natural killer group 2, member D (NKG2D) is an activating receptor present on the surface of natural killer (NK) cells, some NKT cells, CD8⁺ cytotoxic T cells, γδ T cells, and under certain conditions CD4⁺ T cells. Present in both humans and mice, this highly conserved receptor binds to a surprisingly diverse family of ligands that are distant relatives of major histocompatibility complex class I molecules. There is increasing evidence that ligand expression can result in both immune activation (tumor clearance, viral immunity, autoimmunity, and transplantation) and immune silencing (tumor evasion). In this review, we describe this family of NKG2D ligands and the various mechanisms that control their expression in stressed and normal cells. We also discuss the host response to both membrane-bound and secreted NKG2D ligands and summarize the models proposed to explain the consequences of this differential expression.
    Keywords neoplasms ; cytotoxicity ; natural killer cells
    Language English
    Dates of publication 2010-05
    Size p. 267-285.
    Publisher Blackwell Publishing Ltd
    Publishing place Oxford, UK
    Document type Article
    ZDB-ID 391796-4
    ISSN 1600-065X ; 0105-2896
    ISSN (online) 1600-065X
    ISSN 0105-2896
    DOI 10.1111/j.0105-2896.2010.00893.x
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  3. Article: Sensing Bacterial-Induced DNA Damaging Effects

    Espinoza, J Luis / Minami, Mika

    Frontiers in immunology

    2018  Volume 9, Page(s) 52

    Abstract: ... activation is the induction of natural killer group 2 member D ligands (NKG2D-Ls) on the surface of stressed ... of DNA damage agents that may be partially responsible for the overexpression of NKG2D-Ls on intestinal ... cells. Consequently, NKG2D-Ls-expressing cells are recognized and eliminated by NKG2D receptor ...

    Abstract The human genome is constantly exposed to exogenous and endogenous DNA damaging factors that frequently cause DNA damages. Unless repaired, damaged DNA can result in deleterious mutations capable of causing malignant transformation. Accordingly, cells have developed an advanced and effective surveillance system, the DNA damage response (DDR) pathway, which maintains genetic integrity. In addition to well-defined outcomes, such as cell cycle arrest, apoptosis, and senescence, another consequence of DDR activation is the induction of natural killer group 2 member D ligands (NKG2D-Ls) on the surface of stressed cells. Consequently, NKG2D-Ls-expressing cells are recognized and eliminated by NKG2D receptor-expressing immune cells, including NK cells, and various subsets of T-cells. Recent pieces of evidence indicate that commensal microbial imbalance (known as dysbiosis) can trigger DDR activation in host cells, which may result in sustained inflammatory responses. Therefore, dysbiosis can be seen as an important source of DNA damage agents that may be partially responsible for the overexpression of NKG2D-Ls on intestinal epithelial cells that is frequently observed in patients with inflammatory bowel disease and other disorders associated with altered human microbiota, including the development of colorectal cancer. In this article, we discuss recent evidence that appears to link an altered human microbiota with autoimmunity and carcinogenesis
    MeSH term(s) Animals ; Autoimmunity/genetics ; Autoimmunity/immunology ; Bacterial Toxins/immunology ; Carcinogenesis/genetics ; Carcinogenesis/immunology ; Carcinogenesis/metabolism ; DNA Damage ; Dysbiosis ; Gene Expression Regulation ; Humans ; Inflammatory Bowel Diseases/etiology ; Inflammatory Bowel Diseases/metabolism ; Inflammatory Bowel Diseases/pathology ; Microbiota/immunology ; Monitoring, Immunologic ; NK Cell Lectin-Like Receptor Subfamily K/genetics ; NK Cell Lectin-Like Receptor Subfamily K/metabolism
    Chemical Substances Bacterial Toxins ; NK Cell Lectin-Like Receptor Subfamily K
    Language English
    Publishing date 2018-01-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.00052
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: NKG2D expression by CD8+ T cells contributes to GVHD and GVT effects in a murine model of allogeneic HSCT.

    Karimi, Mobin A / Bryson, Jerrod L / Richman, Lee P / Fesnak, Andrew D / Leichner, Theresa M / Satake, Atsushi / Vonderheide, Robert H / Raulet, David H / Reshef, Ran / Kambayashi, Taku

    Blood

    2015  Volume 125, Issue 23, Page(s) 3655–3663

    Abstract: ... T cells. The expression of NKG2D ligands was not induced persistently on normal tissues of allogeneic HSCT ... model of allogeneic HSCT, we hereby demonstrate that NKG2D expression by CD8(+) T cells plays a major ... in those with active GVHD. Together, these data support a novel role for NKG2D expression by CD8(+) T cells during ...

    Abstract In allogeneic hematopoietic stem cell transplantation (HSCT), controlling graft-versus-host disease (GVHD) while maintaining graft-versus-tumor (GVT) responses is of critical importance. Using a mouse model of allogeneic HSCT, we hereby demonstrate that NKG2D expression by CD8(+) T cells plays a major role in mediating GVHD and GVT effects by promoting the survival and cytotoxic function of CD8(+) T cells. The expression of NKG2D ligands was not induced persistently on normal tissues of allogeneic HSCT-recipient mice treated with anti-NKG2D antibody, suggesting that transient NKG2D blockade might be sufficient to attenuate GVHD and allow CD8(+) T cells to regain their GVT function. Indeed, short-term treatment with anti-NKG2D antibody restored GVT effects while maintaining an attenuated GVHD state. NKG2D expression was also detected on CD8(+) T cells from allogeneic HSCT patients and trended to be higher in those with active GVHD. Together, these data support a novel role for NKG2D expression by CD8(+) T cells during allogeneic HSCT, which could be potentially therapeutically exploited to separate GVHD from GVT effects.
    MeSH term(s) Allografts ; Animals ; Antibodies, Neutralizing/pharmacology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/pathology ; Disease Models, Animal ; Gene Expression Regulation/immunology ; Graft vs Host Disease/genetics ; Graft vs Host Disease/immunology ; Graft vs Host Disease/pathology ; Graft vs Tumor Effect/drug effects ; Graft vs Tumor Effect/genetics ; Graft vs Tumor Effect/immunology ; Hematopoietic Stem Cell Transplantation ; Mice ; Mice, Knockout ; NK Cell Lectin-Like Receptor Subfamily K/antagonists & inhibitors ; NK Cell Lectin-Like Receptor Subfamily K/genetics ; NK Cell Lectin-Like Receptor Subfamily K/immunology
    Chemical Substances Antibodies, Neutralizing ; Klrk1 protein, mouse ; NK Cell Lectin-Like Receptor Subfamily K
    Language English
    Publishing date 2015-03-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2015-02-629006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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