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Pesquisa : D12.776.543.750.705.895.800.910 [Categoria DeCS]
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[PMID]:28452850
[Au] Autor:Huang YX; Chen XT; Guo KY; Li YH; Wu BY; Song CY; He YJ
[Ad] Endereço:*Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China †Mount Sinai School of Medicine, Institute of Genomics and Multiscale Biology, New York State University, New York, NY.
[Ti] Título:Sunitinib Induces NK-κB-dependent NKG2D Ligand Expression in Nasopharyngeal Carcinoma and Hepatoma Cells.
[So] Source:J Immunother;40(5):164-174, 2017 Jun.
[Is] ISSN:1537-4513
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multitargeted tyrosine kinase inhibitors (MTKIs) have been shown to combine with natural killer (NK) cell adoptive transfer for the treatment in various cancers. MTKIs sensitize cancer cells to NK cell therapy through upregulation of nature killer group 2 member D ligands (NKG2DLs) on tumor cells. However, the molecular mechanism of MTKIs-mediated upregulation of NKG2DLs is still unknown. In this study, we confirmed sunitinib induced downregulation of its targets, such as vascular endothelial growth factor, platelet-derived growth factor, and c-kit in multiple-drug-resistant nasopharyngeal carcinoma cell line CNE2/DDP and hepatoma cell line HepG2. Then, we further showed sunitinib induced cell proliferation inhibition, apoptosis, and DNA damage in CNE2/DDP and HepG2 cells. Coculture experiments showed that sunitinib-treated CNE2/DDP and HepG2 cells were able to increase the activation and cytotoxicity of NK cells. Quantitative polymerase chain reaction results showed that sunitinib upregulated NKG2DLs, apoptotic genes, DNA damage repair genes, and nuclear factor (NF)-κß family genes. Silencing of NF-κß1, NF-κß2, or RelB (NF-κß pathway) inhibited sunitinib-induced upregulation of NKG2DLs. Taken together, we concluded that sunitinib upregulated NKG2DLs through NF-κß signaling noncanonical pathway which might mediate higher cytotoxic sensitivity of CNE2/DDP and HepG2 cells to NK cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Carcinoma Hepatocelular/metabolismo
Carcinoma/metabolismo
Vigilância Imunológica/efeitos dos fármacos
Indóis/farmacologia
Células Matadoras Naturais/efeitos dos fármacos
Neoplasias Hepáticas/metabolismo
Subfamília K de Receptores Semelhantes a Lectina de Células NK/biossíntese
Neoplasias Nasofaríngeas/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Pirróis/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Carcinoma/terapia
Carcinoma Hepatocelular/terapia
Técnicas de Cocultura
Terapia Combinada
Citotoxicidade Imunológica/efeitos dos fármacos
Expressão Gênica
Células Hep G2
Seres Humanos
Imunoterapia Adotiva
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/transplante
Ligantes
Neoplasias Hepáticas/terapia
NF-kappa B/genética
NF-kappa B/metabolismo
Subfamília K de Receptores Semelhantes a Lectina de Células NK/agonistas
Neoplasias Nasofaríngeas/terapia
RNA Interferente Pequeno/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Indoles); 0 (KLRK1 protein, human); 0 (Ligands); 0 (NF-kappa B); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Protein Kinase Inhibitors); 0 (Pyrroles); 0 (RNA, Small Interfering); V99T50803M (sunitinib)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1097/CJI.0000000000000168


  2 / 1290 MEDLINE  
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[PMID]:28468758
[Au] Autor:Djaoud Z; Guethlein LA; Horowitz A; Azzi T; Nemat-Gorgani N; Olive D; Nadal D; Norman PJ; Münz C; Parham P
[Ad] Endereço:Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305 zdjaoud@stanford.edu peropa@stanford.edu.
[Ti] Título:Two alternate strategies for innate immunity to Epstein-Barr virus: One using NK cells and the other NK cells and γδ T cells.
[So] Source:J Exp Med;214(6):1827-1841, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most humans become infected with Epstein-Barr virus (EBV), which then persists for life. Infrequently, EBV infection causes infectious mononucleosis (IM) or Burkitt lymphoma (BL). Type I EBV infection, particularly type I BL, stimulates strong responses of innate immune cells. Humans respond to EBV in two alternative ways. Of 24 individuals studied, 13 made strong NK and γδ T cell responses, whereas 11 made feeble γδ T cell responses but stronger NK cell responses. The difference does not correlate with sex, HLA type, or previous exposure to EBV or cytomegalovirus. Cohorts of EBV children and pediatric IM patients include both group 1 individuals, with high numbers of γδ T cells, and group 2 individuals, with low numbers. The even balance of groups 1 and 2 in the human population points to both forms of innate immune response to EBV having benefit for human survival. Correlating these distinctive responses with the progress of EBV infection might facilitate the management of EBV-mediated disease.
[Mh] Termos MeSH primário: Herpesvirus Humano 4/imunologia
Imunidade Inata
Células Matadoras Naturais/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Linfócitos B/imunologia
Linfócitos B/virologia
Butirofilinas/metabolismo
Diferenciação Celular/imunologia
Proliferação Celular
Citomegalovirus/fisiologia
Infecções por Vírus Epstein-Barr/imunologia
Infecções por Vírus Epstein-Barr/patologia
Infecções por Vírus Epstein-Barr/virologia
Genótipo
Antígenos HLA/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Fenótipo
Doadores de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (BTN3A1 protein, human); 0 (Butyrophilins); 0 (HLA Antigens); 0 (KLRK1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171206
[Lr] Data última revisão:
171206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161017


  3 / 1290 MEDLINE  
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[PMID]:28947538
[Au] Autor:Vargas-Inchaustegui DA; Helmold Hait S; Chung HK; Narola J; Hoang T; Robert-Guroff M
[Ad] Endereço:Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and.
[Ti] Título:Phenotypic and Functional Characterization of Circulatory, Splenic, and Hepatic NK Cells in Simian Immunodeficiency Virus-Controlling Macaques.
[So] Source:J Immunol;199(9):3202-3211, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NK cells are key components of the immune system because of their rapid response potential and their ability to mediate cytotoxic and immunomodulatory functions. Additionally, NK cells have recently been shown to persist for long periods in vivo and to have the capacity to establish immunologic memory. In the current study, we assessed the phenotype and function of circulatory and tissue-resident NK cells in a unique cohort of SIV-controlling rhesus macaques that maintained low to undetectable levels of viremia in the chronic phase of infection. By contrasting NK responses of these macaques with those observed in SIV-noncontrolling and uninfected macaques, we aimed to identify markers and activities of NK subpopulations associated with disease control. We show in this article that most differences among NK cells of the three groups of macaques were observed in tissue-resident cells. Although SIV infection resulted in NK cell dysfunction, double-negative NK cells and those expressing CXCR3, NKG2D, and IL-18Rα were associated with viremia control, as was Ab-dependent cytotoxic function. Our results suggest several novel targets for therapeutic intervention.
[Mh] Termos MeSH primário: Células Matadoras Naturais/imunologia
Fígado/imunologia
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
Vírus da Imunodeficiência Símia/imunologia
Baço/imunologia
[Mh] Termos MeSH secundário: Animais
Células Matadoras Naturais/patologia
Fígado/patologia
Macaca mulatta
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Receptores CXCR3/imunologia
Síndrome de Imunodeficiência Adquirida dos Símios/patologia
Baço/patologia
Viremia/imunologia
Viremia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700586


  4 / 1290 MEDLINE  
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[PMID]:28893955
[Au] Autor:Sharma N; Trinidad CV; Trembath AP; Markiewicz MA
[Ad] Endereço:Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, KS 66160.
[Ti] Título:NKG2D Signaling between Human NK Cells Enhances TACE-Mediated TNF-α Release.
[So] Source:J Immunol;199(8):2865-2872, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NK group 2 member D (NKG2D) is a strong NK cell-activating receptor, with engagement by ligands triggering granule release and cytokine production. The function of NKG2D signaling in NK cells has largely been studied in the context of engagement of the receptor by ligands expressed on the surface of target cells. We report that upon activation with IL-12, IL-15, and IL-18 human NK cells express NKG2D ligands of the UL16 binding protein family on the cell surface. NKG2D-ligand interaction between cytokine-stimulated NK cells increases the activity of the metalloprotease TNF-α-converting enzyme. This enhanced TNF-α-converting enzyme activity significantly increases the release of TNF-α and UL16 binding protein from the surface of the NK cells. These results demonstrate that NKG2D signaling is critical for maximal TNF-α release by NK cells. Further, they demonstrate a role for NKG2D-ligand interaction via homotypic NK cell contact in NK cell effector function.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Células Matadoras Naturais/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM17/genética
Comunicação Celular
Células Cultivadas
Citotoxicidade Imunológica
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Imunidade Inata
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Interleucina-12/imunologia
Interleucina-15/imunologia
Interleucina-18/imunologia
Ativação Linfocitária
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin-15); 0 (Interleukin-18); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Tumor Necrosis Factor-alpha); 0 (ULBP2 protein, human); 187348-17-0 (Interleukin-12); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700647


  5 / 1290 MEDLINE  
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[PMID]:28802832
[Au] Autor:Streltsova MA; Barsov E; Erokhina SA; Kovalenko EI
[Ad] Endereço:Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, ul. Miklukho-Maklaya, Moscow 117997, Russia. Electronic address: mstreltsova@mail.ru.
[Ti] Título:Retroviral gene transfer into primary human NK cells activated by IL-2 and K562 feeder cells expressing membrane-bound IL-21.
[So] Source:J Immunol Methods;450:90-94, 2017 Nov.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are capable of rapidly recognizing and efficiently killing tumor cells. This makes them a potentially promising agent for cancer immunotherapy. Additional genetic modifications of NK cells may further improve their anti-tumor efficacy. Numerous technical challenges associated with gene delivery into NK cells have significantly tempered this approach. We achieved efficient retroviral vector transduction of primary human NK cells that were stimulated by a combination of IL-2 and engineered K562 cells expressing membrane-bound IL-21. The activated NK cells were in less differentiated state and expressed NK cell activation receptors NKG2D, NKp30, CD16, and were highly HLA-DR-positive. This NK cell population was highly susceptible to the transduction by both GFP- and NGFR-expressing retroviral vectors, with transduction efficiency exceeding 50%. More mature CD57 NK cell population was generally resistant to retroviral vector transduction because of poor response to the stimulation. Our findings may facilitate retroviral vector-mediated genetic engineering of human primary NK cells for future immunotherapies.
[Mh] Termos MeSH primário: Vetores Genéticos
Imunoterapia/métodos
Interleucina-2/metabolismo
Interleucinas/metabolismo
Células Matadoras Naturais/metabolismo
Leucemia Eritroblástica Aguda/terapia
Ativação Linfocitária
Retroviridae/genética
Transdução Genética
Transfecção/métodos
[Mh] Termos MeSH secundário: Antígenos CD57/imunologia
Antígenos CD57/metabolismo
Diferenciação Celular
Técnicas de Cocultura
Células Alimentadoras
Proteínas Ligadas por GPI/imunologia
Proteínas Ligadas por GPI/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Antígenos HLA-DR/imunologia
Antígenos HLA-DR/metabolismo
Seres Humanos
Interleucina-2/imunologia
Interleucinas/imunologia
Células Jurkat
Células K562
Células Matadoras Naturais/imunologia
Leucemia Eritroblástica Aguda/genética
Leucemia Eritroblástica Aguda/imunologia
Leucemia Eritroblástica Aguda/metabolismo
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Receptor 3 Desencadeador da Citotoxicidade Natural/imunologia
Receptor 3 Desencadeador da Citotoxicidade Natural/metabolismo
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Receptores de IgG/imunologia
Receptores de IgG/metabolismo
Receptores de Fator de Crescimento Neural/genética
Receptores de Fator de Crescimento Neural/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD57 Antigens); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (HLA-DR Antigens); 0 (Interleukin-2); 0 (Interleukins); 0 (KLRK1 protein, human); 0 (NCR3 protein, human); 0 (NGFR protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (Nerve Tissue Proteins); 0 (Receptors, IgG); 0 (Receptors, Nerve Growth Factor); 0 (interleukin-21); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE


  6 / 1290 MEDLINE  
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[PMID]:28784848
[Au] Autor:Jensen H; Potempa M; Gotthardt D; Lanier LL
[Ad] Endereço:Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143; and.
[Ti] Título:Cutting Edge: IL-2-Induced Expression of the Amino Acid Transporters SLC1A5 and CD98 Is a Prerequisite for NKG2D-Mediated Activation of Human NK Cells.
[So] Source:J Immunol;199(6):1967-1972, 2017 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Priming of human NK cells with IL-2 is necessary to render them functionally competent upon NKG2D engagement. We examined the underlying mechanisms that control NKG2D responsiveness in NK cells and found that IL-2 upregulates expression of the amino acid transporters SLC1A5 and CD98. Using specific inhibitors to block SLC1A5 and CD98 function, we found that production of IFN-γ and degranulation by CD56 and CD56 NK cells following NKG2D stimulation were dependent on both transporters. IL-2 priming increased the activity of mTORC1, and inhibition of mTORC1 abrogated the ability of the IL-2-primed NK cells to produce IFN-γ in response to NKG2D-mediated stimulation. This study identifies a series of IL-2-induced cellular changes that regulates the NKG2D responsiveness in human NK cells.
[Mh] Termos MeSH primário: Sistema ASC de Transporte de Aminoácidos/metabolismo
Proteína-1 Reguladora de Fusão/metabolismo
Células Matadoras Naturais/fisiologia
Antígenos de Histocompatibilidade Menor/metabolismo
[Mh] Termos MeSH secundário: Sistema ASC de Transporte de Aminoácidos/genética
Antígeno CD56/metabolismo
Células Cultivadas
Citotoxicidade Imunológica
Seres Humanos
Interferon gama/metabolismo
Interleucina-2/imunologia
Interleucina-2/metabolismo
Ativação Linfocitária
Alvo Mecanístico do Complexo 1 de Rapamicina
Antígenos de Histocompatibilidade Menor/genética
Complexos Multiproteicos/antagonistas & inibidores
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Serina-Treonina Quinases TOR/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport System ASC); 0 (CD56 Antigen); 0 (Fusion Regulatory Protein-1); 0 (Interleukin-2); 0 (KLRK1 protein, human); 0 (Minor Histocompatibility Antigens); 0 (Multiprotein Complexes); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (SLC1A5 protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700497


  7 / 1290 MEDLINE  
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[PMID]:28760883
[Au] Autor:Nabekura T; Gotthardt D; Niizuma K; Trsan T; Jenus T; Jonjic S; Lanier LL
[Ad] Endereço:Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143.
[Ti] Título:Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection.
[So] Source:J Immunol;199(5):1567-1571, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NK cells play a critical role in host defense against viruses. In this study, we investigated the role of NKG2D in the expansion of NK cells after mouse CMV (MCMV) infection. Wild-type and NKG2D-deficient ( ) Ly49H NK cells proliferated robustly when infected with MCMV strains engineered to allow expression of NKG2D ligands, which enhanced the response of wild-type NK cells. Naive NK cells exclusively express NKG2D-L, which pairs only with DAP10, whereas NKG2D-S expressed by activated NK cells pairs with DAP10 and DAP12, similar to Ly49H. However, NKG2D alone was unable to drive robust expansion of Ly49H NK cells when mice were infected with these MCMV strains, likely because NKG2D-S was only transiently expressed postinfection. These findings demonstrate that NKG2D augments Ly49H-dependent proliferation of NK cells; however, NKG2D signaling alone is inadequate for expansion of NK cells, likely due to only transient expression of the NKG2D-DAP12 complex.
[Mh] Termos MeSH primário: Infecções por Herpesviridae/imunologia
Células Matadoras Naturais/imunologia
Muromegalovirus/imunologia
Subfamília A de Receptores Semelhantes a Lectina de Células NK/metabolismo
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Proliferação Celular
Células Cultivadas
Imunidade Inata
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Subfamília A de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília K de Receptores Semelhantes a Lectina de Células NK/genética
Ligação Proteica
Receptores Imunológicos/genética
Receptores Imunológicos/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Hcst protein, mouse); 0 (Klra8 protein, mouse); 0 (NK Cell Lectin-Like Receptor Subfamily A); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Receptors, Immunologic); 0 (Tyrobp protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700799


  8 / 1290 MEDLINE  
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[PMID]:28739693
[Au] Autor:Konagai A; Yoshimura K; Hazama S; Yamamoto N; Aoki K; Ueno T; Fujioka M; Iijima H; Kato M; Uchida M; Wada T; Inoue M; Asao T; Fuse M; Wada S; Kuramasu A; Kamei R; Takeda S; Yamamoto S; Yoshino S; Oka M; Nagano H
[Ad] Endereço:Department of Gastroenterological, Breast and Endocrine Surgery, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan.
[Ti] Título:Correlation Between NKG2DL Expression and Antitumor Effect of Protein-bound Polysaccharide-K in Tumor-bearing Mouse Models.
[So] Source:Anticancer Res;37(8):4093-4101, 2017 08.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: We investigated the relationship between the expression of natural killer group 2, member D ligands (NKG2DLs) and the antitumor effects of protein-bound polysaccharide-K (PSK). MATERIALS AND METHODS: PSK was administered to evaluate its effectiveness against tumor growth. The expression of Rae-1 and H60 were analyzed in multiple cell lines. RESULTS: PSK showed the highest antitumor effects in mice implanted with cells expressing neither Rae-1 nor H60. PSK had little antitumor effect in mice implanted with cells expressing both Rae-1 and H60. A correlation between the expression of NKG2DLs and the antitumor effect of PSK was observed. After PSK administration, INF-γ production in CD8 T cells increased in mice with cells expressing neither Rae-1 nor H60, but did not change in mice implanted with cells expressing both Rae-1 and H60. CONCLUSION: We demonstrated that the expression of NKG2DLs affects tumor immunity and the efficacy of immuno therapy in tumor-bearing mouse model.
[Mh] Termos MeSH primário: Proteínas Fúngicas/administração & dosagem
Antígenos de Histocompatibilidade Menor/genética
Subfamília K de Receptores Semelhantes a Lectina de Células NK/genética
Neoplasias/tratamento farmacológico
Proteínas Associadas à Matriz Nuclear/genética
Proteínas de Transporte Nucleocitoplasmático/genética
Polissacarídeos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Ligantes
Camundongos
Antígenos de Histocompatibilidade Menor/biossíntese
Subfamília K de Receptores Semelhantes a Lectina de Células NK/biossíntese
Neoplasias/genética
Neoplasias/patologia
Proteínas Associadas à Matriz Nuclear/biossíntese
Proteínas de Transporte Nucleocitoplasmático/biossíntese
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungal Proteins); 0 (KLRK1 protein, human); 0 (Ligands); 0 (Minor Histocompatibility Antigens); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Nuclear Matrix-Associated Proteins); 0 (Nucleocytoplasmic Transport Proteins); 0 (Polysaccharides); 0 (RAE1 protein, human); 0 (minor H antigen H60); 0 (protein-bound polysaccharide K, Basidiomycetes)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28708284
[Au] Autor:Peipp M; Wesch D; Oberg HH; Lutz S; Muskulus A; van de Winkel JGJ; Parren PWHI; Burger R; Humpe A; Kabelitz D; Gramatzki M; Kellner C
[Ad] Endereço:Division of Stem Cell Transplantation and Immunotherapy, 2nd Department of Medicine, Christian-Albrechts-University of Kiel, Kiel, Germany.
[Ti] Título:CD20-Specific Immunoligands Engaging NKG2D Enhance γδ T Cell-Mediated Lysis of Lymphoma Cells.
[So] Source:Scand J Immunol;86(4):196-206, 2017 Oct.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human γδ T cells are innate-like T cells which are able to kill a broad range of tumour cells and thus may have potential for cancer immunotherapy. The activating receptor natural killer group 2 member D (NKG2D) plays a key role in regulating immune responses driven by γδ T cells. Here, we explored whether recombinant immunoligands consisting of a CD20 single-chain fragment variable (scFv) linked to a NKG2D ligand, either MHC class I chain-related protein A (MICA) or UL16 binding protein 2 (ULBP2), could be employed to engage γδ T cells for tumour cell killing. The two immunoligands, designated MICA:7D8 and ULBP2:7D8, respectively, enhanced cytotoxicity of ex vivo-expanded γδ T cells against CD20-positive lymphoma cells. Both Vδ1 and Vδ2 γδ T cells were triggered by MICA:7D8 or ULBP2:7D8. Killing of CD20-negative tumour cells was not induced by the immunoligands, indicating their antigen specificity. MICA:7D8 and ULBP2:7D8 acted in a dose-dependent manner and induced cytotoxicity at nanomolar concentrations. Importantly, chronic lymphocytic leukaemia (CLL) cells isolated from patients were sensitized by the two immunoligands for γδ T cell cytotoxicity. In a combination approach, the immunoligands were combined with bromohydrin pyrophosphate (BrHPP), an agonist for Vδ2 γδ T cells, which further enhanced the efficacy in target cell killing. Thus, employing tumour-directed recombinant immunoligands which engage NKG2D may represent an attractive strategy to enhance antitumour cytotoxicity of γδ T cells.
[Mh] Termos MeSH primário: Antígenos CD20/metabolismo
Citotoxicidade Imunológica
Imunoterapia/métodos
Linfoma/terapia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Anticorpos de Cadeia Única/uso terapêutico
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Antígenos CD20/imunologia
Difosfatos/uso terapêutico
Quimioterapia Combinada
Proteínas Ligadas por GPI/genética
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Imunização
Peptídeos e Proteínas de Sinalização Intercelular/genética
Linfoma/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Anticorpos de Cadeia Única/genética
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD20); 0 (Diphosphates); 0 (GPI-Linked Proteins); 0 (Histocompatibility Antigens Class I); 0 (Intercellular Signaling Peptides and Proteins); 0 (KLRK1 protein, human); 0 (MHC class I-related chain A); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Single-Chain Antibodies); 0 (ULBP2 protein, human); 0 (bromohydrin pyrophosphate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12581


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[PMID]:28689087
[Au] Autor:Desimio MG; Giuliani E; Doria M
[Ad] Endereço:Laboratory of Immunoinfectivology, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
[Ti] Título:The histone deacetylase inhibitor SAHA simultaneously reactivates HIV-1 from latency and up-regulates NKG2D ligands sensitizing for natural killer cell cytotoxicity.
[So] Source:Virology;510:9-21, 2017 Oct.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In pilot HIV-1 eradication studies, patients' immune responses were ineffective at killing viral reservoirs reactivated through latency reversing agents (LRAs) like suberoylanilide hydroxamic acid (SAHA). We hypothesized that T cells harboring reactivated HIV-1 express MIC and ULBP ligands for the activating NKG2D receptor of natural killer (NK) cells. Here, we demonstrated that MICA/B and ULBP2 are induced by SAHA on primary T cells harboring reactivated virus. Using latently HIV-1-infected J-Lat 6.3/8.4/9.2 and J1.1 cell lines, we showed that SAHA reverts latency and, simultaneously, up-regulates MICA/B and ULBP2 acting at the transcriptional level and through ATR activation, thus sensitizing T cells with reactivated virus to NKG2D-mediated killing by NK cells. Moreover, IL-2 and IL-15 potently boosted NKG2D expression and cytotoxicity of NK cells against SAHA-reactivated p24 target cells. Therefore, immunotherapy with cytokines enhancing NKG2D-mediated NK-cell cytotoxicity combined with administration of LRAs up-modulating NKG2D ligands, represents a promising approach towards HIV-1 eradication.
[Mh] Termos MeSH primário: HIV-1/fisiologia
Inibidores de Histona Desacetilases/metabolismo
Ácidos Hidroxâmicos/metabolismo
Células Matadoras Naturais/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/biossíntese
Latência Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células Cultivadas
Proteínas Ligadas por GPI/análise
Perfilação da Expressão Gênica
Infecções por HIV/terapia
Antígenos de Histocompatibilidade Classe I/análise
Seres Humanos
Imunoterapia/métodos
Peptídeos e Proteínas de Sinalização Intercelular/análise
Linfócitos T/efeitos dos fármacos
Linfócitos T/virologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GPI-Linked Proteins); 0 (Histocompatibility Antigens Class I); 0 (Histone Deacetylase Inhibitors); 0 (Hydroxamic Acids); 0 (Intercellular Signaling Peptides and Proteins); 0 (KLRK1 protein, human); 0 (MHC class I-related chain A); 0 (MICB antigen); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (ULBP2 protein, human); 58IFB293JI (vorinostat)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE



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