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[PMID]:28746740
[Au] Autor:McDonald KG; Wheeler LW; McDole JR; Joerger S; Gustafsson JK; Kulkarni DH; Knoop KA; Williams IR; Miller MJ; Newberry RD
[Ad] Endereço:Department of Internal Medicine, Washington University School of Medicine, St Louis, MO, USA.
[Ti] Título:CCR6 promotes steady-state mononuclear phagocyte association with the intestinal epithelium, imprinting and immune surveillance.
[So] Source:Immunology;152(4):613-627, 2017 12.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The intestinal lamina propria (LP) contains antigen-presenting cells with features of dendritic cells and macrophages, collectively referred to as mononuclear phagocytes (MNPs). Association of MNPs with the epithelium is thought to play an important role in multiple facets of intestinal immunity including imprinting MNPs with the ability to induce IgA production, inducing the expression of gut homing molecules on T cells, facilitating the capture of luminal antigens and microbes, and subsequent immune responses in the mesenteric lymph node (MLN). However, the factors promoting this process in the steady state are largely unknown, and in vivo models to test and confirm the importance of LP-MNP association with the epithelium for these outcomes are unexplored. Evaluation of epithelial expression of chemoattractants in mice where MNP-epithelial associations were impaired suggested CCL20 as a candidate promoting epithelial association. Expression of CCR6, the only known receptor for CCL20, was required for MNPs to associate with the epithelium. LP-MNPs from CCR6 mice did not display defects in acquiring antigen and stimulating T-cell responses in ex vivo assays or in responses to antigen administered systemically. However, LP-MNPs from CCR6-deficient mice were impaired at acquiring luminal and epithelial antigens, inducing IgA production in B cells, inducing immune responses in the MLN, and capturing and trafficking luminal commensal bacteria to the MLN. These findings identify a crucial role for CCR6 in promoting LP-MNPs to associate with the intestinal epithelium in the steady state to perform multiple functions promoting gut immune homeostasis.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Impressão Genômica/imunologia
Vigilância Imunológica
Mucosa Intestinal/imunologia
Macrófagos/imunologia
Receptores CCR6/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Linfócitos B/imunologia
Quimiocina CCL20/genética
Quimiocina CCL20/imunologia
Células Dendríticas/citologia
Seres Humanos
Macrófagos/citologia
Camundongos
Camundongos Knockout
Receptores CCR6/genética
Linfócitos T/citologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CCL20 protein, mouse); 0 (CCR6 protein, mouse); 0 (Chemokine CCL20); 0 (Receptors, CCR6)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12801


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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


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[PMID]:28465341
[Au] Autor:Gorini F; Azzimonti L; Delfanti G; Scarfò L; Scielzo C; Bertilaccio MT; Ranghetti P; Gulino A; Doglioni C; Di Napoli A; Capri M; Franceschi C; Caligaris-Cappio F; Ghia P; Bellone M; Dellabona P; Casorati G; de Lalla C
[Ad] Endereço:Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy.
[Ti] Título:Invariant NKT cells contribute to chronic lymphocytic leukemia surveillance and prognosis.
[So] Source:Blood;129(26):3440-3451, 2017 06 29.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic lymphocytic leukemia (CLL) is characterized by the expansion of malignant CD5 B lymphocytes in blood, bone marrow, and lymphoid organs. CD1d-restricted invariant natural killer T (iNKT) cells are innate-like T lymphocytes strongly implicated in tumor surveillance. We investigated the impact of iNKT cells in the natural history of the disease in the Eµ-Tcl1 (Tcl1) CLL mouse model and 68 CLL patients. We found that Tcl1-CLL cells express CD1d and that iNKT cells critically delay disease onset but become functionally impaired upon disease progression. In patients, disease progression correlates with high CD1d expression on CLL cells and impaired iNKT cells. Conversely, disease stability correlates with negative or low CD1d expression on CLL cells and normal iNKT cells, suggesting indirect leukemia control. iNKT cells indeed hinder CLL survival in vitro by restraining CD1d-expressing nurse-like cells, a relevant proleukemia macrophage population. Multivariable analysis identified iNKT cell frequency as an independent predictor of disease progression. Together, these results support the contribution of iNKT cells to CLL immune surveillance and highlight iNKT cell frequency as a prognostic marker for disease progression.
[Mh] Termos MeSH primário: Vigilância Imunológica
Leucemia Linfocítica Crônica de Células B/imunologia
Células T Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Antígenos CD1d/sangue
Progressão da Doença
Feminino
Seres Humanos
Leucemia Linfocítica Crônica de Células B/patologia
Contagem de Linfócitos
Masculino
Camundongos
Meia-Idade
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (CD1D protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-751065


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[PMID]:28922404
[Au] Autor:Quintero V JC; Paternina T LE; Uribe Y A; Muskus C; Hidalgo M; Gil J; Cienfuegos G AV; Osorio Q L; Rojas A C
[Ad] Endereço:Grupo de Ciencias Veterinarias - Centauro, Facultad de Ciencias Agrarias, Universidad de Antioquia, Medellín, Colombia.
[Ti] Título:Eco-epidemiological analysis of rickettsial seropositivity in rural areas of Colombia: A multilevel approach.
[So] Source:PLoS Negl Trop Dis;11(9):e0005892, 2017 Sep.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rickettsiosis is a re-emergent infectious disease without epidemiological surveillance in Colombia. This disease is generally undiagnosed and several deadly outbreaks have been reported in the country in the last decade. The aim of this study is to analyze the eco-epidemiological aspects of rickettsial seropositivity in rural areas of Colombia where outbreaks of the disease were previously reported. A cross-sectional study, which included 597 people living in 246 households from nine hamlets in two municipalities of Colombia, was conducted from November 2015 to January 2016. The survey was conducted to collect sociodemographic and household characteristics (exposure) data. Blood samples were collected to determine the rickettsial seropositivity in humans, horses and dogs (IFA, cut-off = 1/128). In addition, infections by rickettsiae were detected in ticks from humans and animals by real-time PCR targeting gltA and ompA genes. Data was analyzed by weighted multilevel clog-log regression model using three levels (person, household and hamlets) and rickettsial seropositivity in humans was the main outcome. Overall prevalence of rickettsial seropositivity in humans was 25.62% (95%CI 22.11-29.12). Age in years (PR = 1.01 95%CI 1.01-1.02) and male sex (PR = 1.65 95%CI 1.43-1.90) were risk markers for rickettsial seropositivity. Working outdoors (PR = 1.20 95%CI 1.02-1.41), deforestation and forest fragmentation for agriculture use (PR = 1.75 95%CI 1.51-2.02), opossum in peridomiciliary area (PR = 1.56 95%CI 1.37-1.79) and a high proportion of seropositive domestic animals in the home (PR20-40% vs <20% = 2.28 95%CI 1.59-3.23 and PR>40% vs <20% = 3.14 95%CI 2.43-4.04) were associated with rickettsial seropositivity in humans. This study showed the presence of Rickettsia antibodies in human populations and domestic animals. In addition, different species of rickettsiae were detected in ticks collected from humans and animals. Our results highlighted the role of domestic animals as sentinels of rickettsial infection to identify areas at risk of transmission, and the importance of preventive measures aimed at curtailing deforestation and the fragmentation of forests as a way of reducing the risk of transmission of emergent and re-emergent pathogens.
[Mh] Termos MeSH primário: Anticorpos Antibacterianos/sangue
Ecossistema
Vigilância Imunológica
Infecções por Rickettsia/epidemiologia
Infecções por Rickettsia/imunologia
Rickettsia/imunologia
Carrapatos/microbiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Animais Domésticos/microbiologia
Colômbia/epidemiologia
Conservação dos Recursos Naturais
Estudos Transversais
Doenças do Cão/epidemiologia
Doenças do Cão/imunologia
Doenças do Cão/microbiologia
Cães
Características da Família
Feminino
Doenças dos Cavalos/epidemiologia
Doenças dos Cavalos/imunologia
Doenças dos Cavalos/microbiologia
Cavalos/imunologia
Cavalos/microbiologia
Seres Humanos
Masculino
Meia-Idade
Prevalência
Rickettsia/isolamento & purificação
Infecções por Rickettsia/transmissão
Infecções por Rickettsia/veterinária
Fatores de Risco
População Rural
Estudos Soroepidemiológicos
Infestações por Carrapato/epidemiologia
Infestações por Carrapato/veterinária
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Bacterial)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005892


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[PMID]:28891811
[Au] Autor:Ratnam NM; Peterson JM; Talbert EE; Ladner KJ; Rajasekera PV; Schmidt CR; Dillhoff ME; Swanson BJ; Haverick E; Kladney RD; Williams TM; Leone GW; Wang DJ; Guttridge DC
[Ad] Endereço:Department of Cancer Biology and Genetics.
[Ti] Título:NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development.
[So] Source:J Clin Invest;127(10):3796-3809, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macrophages are attracted to developing tumors and can participate in immune surveillance to eliminate neoplastic cells. In response, neoplastic cells utilize NF-κB to suppress this killing activity, but the mechanisms underlying their self-protection remain unclear. Here, we report that this dynamic interaction between tumor cells and macrophages is integrally linked by a soluble factor identified as growth and differentiation factor 15 (GDF-15). In vitro, tumor-derived GDF-15 signals in macrophages to suppress their proapoptotic activity by inhibiting TNF and nitric oxide (NO) production. In vivo, depletion of GDF-15 in Ras-driven tumor xenografts and in an orthotopic model of pancreatic cancer delayed tumor development. This delay correlated with increased infiltrating antitumor macrophages. Further, production of GDF-15 is directly regulated by NF-κB, and the colocalization of activated NF-κB and GDF-15 in epithelial ducts of human pancreatic adenocarcinoma supports the importance of this observation. Mechanistically, we found that GDF-15 suppresses macrophage activity by inhibiting TGF-ß-activated kinase (TAK1) signaling to NF-κB, thereby blocking synthesis of TNF and NO. Based on these results, we propose that the NF-κB/GDF-15 regulatory axis is important for tumor cells in evading macrophage immune surveillance during the early stages of tumorigenesis.
[Mh] Termos MeSH primário: Adenocarcinoma/imunologia
Fator 15 de Diferenciação de Crescimento/imunologia
Vigilância Imunológica
Macrófagos/imunologia
NF-kappa B/imunologia
Proteínas de Neoplasias/imunologia
Neoplasias Experimentais/imunologia
Neoplasias Pancreáticas/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/patologia
Animais
Feminino
Fator 15 de Diferenciação de Crescimento/genética
Xenoenxertos
MAP Quinase Quinase Quinases
Macrófagos/patologia
Masculino
Camundongos
Camundongos Knockout
NF-kappa B/genética
Proteínas de Neoplasias/genética
Transplante de Neoplasias
Neoplasias Experimentais/genética
Neoplasias Experimentais/patologia
Óxido Nítrico/genética
Óxido Nítrico/imunologia
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Transdução de Sinais/genética
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GDF15 protein, human); 0 (Growth Differentiation Factor 15); 0 (NF-kappa B); 0 (Neoplasm Proteins); 0 (Tumor Necrosis Factor-alpha); 31C4KY9ESH (Nitric Oxide); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE


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[PMID]:28810142
[Au] Autor:López-Soto A; Gonzalez S; Smyth MJ; Galluzzi L
[Ad] Endereço:Departamento de Biología Funcional, Área de Inmunología, Universidad de Oviedo, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), 33006 Oviedo, Asturias, Spain. Electronic address: lopezsalejandro@uniovi.es.
[Ti] Título:Control of Metastasis by NK Cells.
[So] Source:Cancer Cell;32(2):135-154, 2017 Aug 14.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The metastatic spread of malignant cells to distant anatomical locations is a prominent cause of cancer-related death. Metastasis is governed by cancer-cell-intrinsic mechanisms that enable neoplastic cells to invade the local microenvironment, reach the circulation, and colonize distant sites, including the so-called epithelial-to-mesenchymal transition. Moreover, metastasis is regulated by microenvironmental and systemic processes, such as immunosurveillance. Here, we outline the cancer-cell-intrinsic and -extrinsic factors that regulate metastasis, discuss the key role of natural killer (NK) cells in the control of metastatic dissemination, and present potential therapeutic approaches to prevent or target metastatic disease by harnessing NK cells.
[Mh] Termos MeSH primário: Células Matadoras Naturais/imunologia
Metástase Neoplásica/imunologia
Neoplasias/prevenção & controle
Microambiente Tumoral
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Vigilância Imunológica
Imunoterapia
Metástase Neoplásica/patologia
Metástase Neoplásica/prevenção & controle
Neoplasias/imunologia
Neoplasias/patologia
Evasão Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28779024
[Au] Autor:Audemard-Verger A; Rivière M; Durand A; Peranzoni E; Guichard V; Hamon P; Bonilla N; Guilbert T; Boissonnas A; Auffray C; Eberl G; Lucas B; Martin B
[Ad] Endereço:Institut Cochin, CNRS UMR8104, INSERM U1016, Paris Descartes Université, 75014 Paris, France.
[Ti] Título:Macrophages Induce Long-Term Trapping of γδ T Cells with Innate-like Properties within Secondary Lymphoid Organs in the Steady State.
[So] Source:J Immunol;199(6):1998-2007, 2017 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:So far, peripheral T cells have mostly been described to circulate between blood, secondary lymphoid organs (SLOs), and lymph in the steady state. This nomadic existence would allow them to accomplish their surveying task for both foreign Ags and survival signals. Although it is now well established that γδ T cells can be rapidly recruited to inflammatory sites or in certain tumor microenvironments, the trafficking properties of peripheral γδ T cells have been poorly studied in the steady state. In the present study, we highlight the existence of resident γδ T cells in the SLOs of specific pathogen-free mice. Indeed, using several experimental approaches such as the injection of integrin-neutralizing Abs that inhibit the entry of circulating lymphocytes into lymph nodes and long-term parabiosis experiments, we have found that, contrary to Ly-6C CD44 and Ly-6C CD44 γδ T cells, a significant proportion of Ly-6C CD44 γδ T cells are trapped for long periods of time within lymph nodes and the spleen in the steady state. Specific in vivo cell depletion strategies have allowed us to demonstrate that macrophages are the main actors involved in this long-term retention of Ly-6C CD44 γδ T cells in SLOs.
[Mh] Termos MeSH primário: Linfonodos/imunologia
Macrófagos/imunologia
Baço/imunologia
Subpopulações de Linfócitos T/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/metabolismo
Comunicação Celular
Movimento Celular
Células Cultivadas
Receptores de Hialuronatos/metabolismo
Imunidade Inata
Vigilância Imunológica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Hyaluronan Receptors); 0 (Ly-6C antigen, mouse); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[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:170806
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700430


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[PMID]:28581441
[Au] Autor:Putz EM; Mayfosh AJ; Kos K; Barkauskas DS; Nakamura K; Town L; Goodall KJ; Yee DY; Poon IK; Baschuk N; Souza-Fonseca-Guimaraes F; Hulett MD; Smyth MJ
[Ad] Endereço:Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.
[Ti] Título:NK cell heparanase controls tumor invasion and immune surveillance.
[So] Source:J Clin Invest;127(7):2777-2788, 2017 Jun 30.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NK cells are highly efficient at preventing cancer metastasis but are infrequently found in the core of primary tumors. Here, have we demonstrated that freshly isolated mouse and human NK cells express low levels of the endo-ß-D-glucuronidase heparanase that increase upon NK cell activation. Heparanase deficiency did not affect development, differentiation, or tissue localization of NK cells under steady-state conditions. However, mice lacking heparanase specifically in NK cells (Hpsefl/fl NKp46-iCre mice) were highly tumor prone when challenged with the carcinogen methylcholanthrene (MCA). Hpsefl/fl NKp46-iCre mice were also more susceptible to tumor growth than were their littermate controls when challenged with the established mouse lymphoma cell line RMA-S-RAE-1ß, which overexpresses the NK cell group 2D (NKG2D) ligand RAE-1ß, or when inoculated with metastatic melanoma, prostate carcinoma, or mammary carcinoma cell lines. NK cell invasion of primary tumors and recruitment to the site of metastasis were strictly dependent on the presence of heparanase. Cytokine and immune checkpoint blockade immunotherapy for metastases was compromised when NK cells lacked heparanase. Our data suggest that heparanase plays a critical role in NK cell invasion into tumors and thereby tumor progression and metastases. This should be considered when systemically treating cancer patients with heparanase inhibitors, since the potential adverse effect on NK cell infiltration might limit the antitumor activity of the inhibitors.
[Mh] Termos MeSH primário: Heparina Liase/imunologia
Vigilância Imunológica
Células Matadoras Naturais/imunologia
Neoplasias Experimentais/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Citocinas/genética
Citocinas/imunologia
Feminino
Heparina Liase/genética
Seres Humanos
Células Matadoras Naturais/patologia
Masculino
Camundongos
Camundongos Knockout
Subfamília K de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Invasividade Neoplásica/genética
Invasividade Neoplásica/imunologia
Metástase Neoplásica
Neoplasias Experimentais/genética
Neoplasias Experimentais/patologia
Proteínas Associadas à Matriz Nuclear/genética
Proteínas Associadas à Matriz Nuclear/imunologia
Proteínas de Transporte Nucleocitoplasmático/genética
Proteínas de Transporte Nucleocitoplasmático/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (KLRK1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Nuclear Matrix-Associated Proteins); 0 (Nucleocytoplasmic Transport Proteins); 0 (RAE1 protein, human); EC 4.2.2.7 (Heparin Lyase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170930
[Lr] Data última revisão:
170930
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE


  9 / 1449 MEDLINE  
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[PMID]:28566372
[Au] Autor:Saito T; Yano M; Ohki Y; Tomura M; Nakano N
[Ad] Endereço:Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba 278-0022, Japan; and.
[Ti] Título:Occludin Expression in Epidermal γδ T Cells in Response to Epidermal Stress Causes Them To Migrate into Draining Lymph Nodes.
[So] Source:J Immunol;199(1):62-71, 2017 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidermal γδ T cells that reside in the front line of the skin play a pivotal role in stress immune surveillance. However, it is not clear whether these cells are involved in further induction of immune responses after they are activated in dysregulated epidermis. In this study, we found that activated γδ T cells expressed occludin and migrated into draining lymph nodes in an occludin-dependent manner. Epidermal γδ T cells in occludin-deficient mice exhibited impairments in morphology changes and motility, although they expressed activation markers at levels comparable to those in wild-type cells. Occludin deficiency weakened the induction of allergen-induced contact hypersensitivity, primarily as the result of the impaired migration of epidermal γδ T cells. Thus, occludin expression by epidermal γδ T cells upon activation in response to epidermal stress allows them to move, which could be important for augmentation of immune responses via collaboration with other cells.
[Mh] Termos MeSH primário: Movimento Celular
Epiderme/imunologia
Linfonodos/imunologia
Ocludina/genética
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Estresse Fisiológico
Subpopulações de Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Dermatite de Contato/imunologia
Epiderme/citologia
Epiderme/efeitos da radiação
Vigilância Imunológica
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Pele/imunologia
Subpopulações de Linfócitos T/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Occludin); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600848


  10 / 1449 MEDLINE  
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[PMID]:28539110
[Au] Autor:Melief CJM; Kessler JH
[Ad] Endereço:ISA Pharmaceuticals, J.H. Oortweg 19, 2333 CH, Leiden, The Netherlands. melief@isa-pharma.com.
[Ti] Título:Novel insights into the HLA class I immunopeptidome and T-cell immunosurveillance.
[So] Source:Genome Med;9(1):44, 2017 May 24.
[Is] ISSN:1756-994X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Advances in mass spectrometry have allowed the high-throughput quantitative identification of human leukocyte antigen (HLA) class I ligands, and recent studies have reported on the breadth and diversity of the HLA class I immunopeptidome. These findings have far-reaching implications for immunosurveillance by T cells and translational value for immunotherapy.
[Mh] Termos MeSH primário: Antígenos de Histocompatibilidade Classe I
Vigilância Imunológica
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Imunoterapia
Linfócitos T/imunologia
[Pt] Tipo de publicação:EDITORIAL; REVIEW
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1186/s13073-017-0439-8



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