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[PMID]:27565739
[Au] Autor:Walter L; Petersen B
[Ad] Endereço:Primate Genetics Laboratory, Leibniz Institute for Primate Research, German Primate Center, Göttingen, Germany.
[Ti] Título:Diversification of both KIR and NKG2 natural killer cell receptor genes in macaques - implications for highly complex MHC-dependent regulation of natural killer cells.
[So] Source:Immunology;150(2):139-145, 2017 Feb.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The killer immunoglobulin-like receptors (KIR) as well as their MHC class I ligands display enormous genetic diversity and polymorphism in macaque species. Signals resulting from interaction between KIR or CD94/NKG2 receptors and their cognate MHC class I proteins essentially regulate the activity of natural killer (NK) cells. Macaque and human KIR share many features, such as clonal expression patterns, gene copy number variations, specificity for particular MHC class I allotypes, or epistasis between KIR and MHC class I genes that influence susceptibility and resistance to immunodeficiency virus infection. In this review article we also annotated publicly available rhesus macaque BAC clone sequences and provide the first description of the CD94-NKG2 genomic region. Besides the presence of genes that are orthologous to human NKG2A and NKG2F, this region contains three NKG2C paralogues. Hence, the genome of rhesus macaques contains moderately expanded and diversified NKG2 genes in addition to highly diversified KIR genes. The presence of two diversified NK cell receptor families in one species has not been described before and is expected to require a complex MHC-dependent regulation of NK cells.
[Mh] Termos MeSH primário: Células Matadoras Naturais/fisiologia
Macaca
Subfamília C de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília D de Receptores Semelhantes a Lectina de Células NK/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Animais
Evolução Molecular
Antígenos de Histocompatibilidade Classe I/metabolismo
Seres Humanos
Imunidade/genética
Filogenia
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Receptors, KIR)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170517
[Lr] Data última revisão:
170517
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12666


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[PMID]:27965986
[Au] Autor:Sairafi D; Stikvoort A; Gertow J; Mattsson J; Uhlin M
[Ad] Endereço:Centre for Allogeneic Stem Cell Transplantation, Karolinska University Hospital, Huddinge, Sweden.
[Ti] Título:Donor Cell Composition and Reactivity Predict Risk of Acute Graft-versus-Host Disease after Allogeneic Hematopoietic Stem Cell Transplantation.
[So] Source:J Immunol Res;2016:5601204, 2016.
[Is] ISSN:2314-7156
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:. Graft-versus-host disease (GVHD) is a serious complication after allogeneic hematopoietic stem cell transplantation (HSCT). We designed a functional assay for assessment of individual risk for acute GVHD. . Blood samples were collected from patients and donors before HSCT. Two groups of seven patients each were selected, one in which individuals developed acute GVHD grades II-IV and one in which none showed any clinical signs of GVHD. Peripheral blood mononuclear cells (PBMCs) isolated from donors were incubated in mixed lymphocyte cultures (MLCs) with recipient PBMCs. The cells were characterized by flow cytometry before and after MLC. . Samples from donors in the GVHD group contained significantly lower frequencies of naïve T-cells and T-cells expressing NK-cell markers CD56 and CD94. Donor samples in this group also exhibited lower frequencies of naïve CD95 T-cells compared to controls. After MLC, there were dissimilarities in the CD4/CD8 T-cell ratio and frequency of CD69 T-cells between the two patient groups, with the non-GVHD group showing higher frequencies of CD8 and CD69 T-cells. . We conclude that a thorough flow cytometric analysis of donor cells for phenotype and allogeneic reactivity may be of value when assessing pretransplant risk for severe acute GVHD.
[Mh] Termos MeSH primário: Doença Enxerto-Hospedeiro/etiologia
Doença Enxerto-Hospedeiro/prevenção & controle
Transplante de Células-Tronco Hematopoéticas
Leucócitos Mononucleares/imunologia
Subpopulações de Linfócitos T/imunologia
Doadores de Tecidos
[Mh] Termos MeSH secundário: Doença Aguda
Adolescente
Adulto
Relação CD4-CD8
Antígeno CD56/imunologia
Feminino
Citometria de Fluxo
Doença Enxerto-Hospedeiro/imunologia
Seres Humanos
Leucócitos Mononucleares/citologia
Teste de Cultura Mista de Linfócitos
Masculino
Meia-Idade
Subfamília D de Receptores Semelhantes a Lectina de Células NK/imunologia
Fatores de Risco
Transplante Homólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD56 Antigen); 0 (KLRD1 protein, human); 0 (NCAM1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily D)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161215
[St] Status:MEDLINE


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[PMID]:27801784
[Au] Autor:Kordelas L; Steckel NK; Horn PA; Beelen DW; Rebmann V
[Ad] Endereço:Department of Bone Marrow Transplantation, University Hospital Essen, Essen 45147, Germany. lambros.kordelas@uk-essen.de.
[Ti] Título:The Activating NKG2C Receptor Is Significantly Reduced in NK Cells after Allogeneic Stem Cell Transplantation in Patients with Severe Graft-versus-Host Disease.
[So] Source:Int J Mol Sci;17(11), 2016 Oct 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells play a central role in the innate immune system. In allogeneic stem cell transplantation (alloSCT), alloreactive NK cells derived by the graft are discussed to mediate the elimination of leukemic cells and dendritic cells in the patient and thereby to reduce the risk for leukemic relapses and graft-versus-host reactions. The alloreactivity of NK cells is determined by various receptors including the activating CD94/NKG2C and the inhibitory CD94/NKG2A receptors, which both recognize the non-classical human leukocyte antigen E (HLA-E). Here we analyze the contribution of these receptors to NK cell alloreactivity in 26 patients over the course of the first year after alloSCT due to acute myeloid leukemia, myelodysplastic syndrome and T cell Non-Hodgkin-Lymphoma. Our results show that NK cells expressing the activating CD94/NKG2C receptor are significantly reduced in patients after alloSCT with severe acute and chronic graft-versus-host disease (GvHD). Moreover, the ratio of CD94/NKG2C to CD94/NKG2A was reduced in patients with severe acute and chronic GvHD after receiving an HLA-mismatched graft. Collectively, these results provide evidence for the first time that CD94/NKG2C is involved in GvHD prevention.
[Mh] Termos MeSH primário: Doença Enxerto-Hospedeiro/imunologia
Leucemia Mieloide Aguda/imunologia
Linfoma não Hodgkin/imunologia
Síndromes Mielodisplásicas/imunologia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/biossíntese
Subfamília D de Receptores Semelhantes a Lectina de Células NK/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Doença Enxerto-Hospedeiro/patologia
Doença Enxerto-Hospedeiro/prevenção & controle
Antígenos de Histocompatibilidade Classe I/imunologia
Seres Humanos
Imunidade Inata/genética
Células Matadoras Naturais/imunologia
Leucemia Mieloide Aguda/patologia
Leucemia Mieloide Aguda/terapia
Linfoma não Hodgkin/patologia
Linfoma não Hodgkin/terapia
Masculino
Meia-Idade
Síndromes Mielodisplásicas/patologia
Síndromes Mielodisplásicas/terapia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/imunologia
Subfamília D de Receptores Semelhantes a Lectina de Células NK/imunologia
Transplante de Células-Tronco/efeitos adversos
Transplante Homólogo/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HLA-E antigen); 0 (Histocompatibility Antigens Class I); 0 (KLRD1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily D)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE


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[PMID]:27720695
[Au] Autor:Li XP; Hu YH
[Ad] Endereço:Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China; Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao, China; University of Chinese Academy of Sciences, Beijing, China.
[Ti] Título:CD94 of tongue sole Cynoglossus semilaevis binds a wide arrange of bacteria and possesses antibacterial activity.
[So] Source:Fish Shellfish Immunol;58:641-649, 2016 Nov.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, we examined the expression patterns and the functions of the tongue sole Cynoglossus semilaevis CD94, CsCD94. CsCD94 is composed of 209 amino acid residues and shares 43.0-50.2% overall identities with known teleost CD94 sequence. CsCD94 has a C-type lectin-like domain. Expression of CsCD94 occurred in multiple tissues and was upregulated during bacterial infection. Recombinant CsCD94 (rCsCD94) exhibited apparent binding and agglutinating activities against both Gram-positive and Gram-negative bacteria in a Ca -dependent manner. Treatment of bacteria with rCsCD94 enhanced phagocytosis of the bacteria by peripheral blood leukocytes. Furthermore, incubation of rCsCD94 with bacteria reduced the survival of the bacteria in vitro. Taken together, these results indicate that rCsCD94 is a key factor in the bactericidal and phagocytic effects of tongue sole, and reveal for the first time an essential role of fish CD94 in antibacterial immunity, thereby adding insight into the function of CD94.
[Mh] Termos MeSH primário: Doenças dos Peixes/genética
Proteínas de Peixes/genética
Linguados
Expressão Gênica
Imunidade Inata
Subfamília D de Receptores Semelhantes a Lectina de Células NK/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
DNA Complementar/genética
DNA Complementar/metabolismo
Doenças dos Peixes/imunologia
Doenças dos Peixes/microbiologia
Proteínas de Peixes/química
Proteínas de Peixes/metabolismo
Bactérias Gram-Negativas/fisiologia
Infecções por Bactérias Gram-Negativas/genética
Infecções por Bactérias Gram-Negativas/imunologia
Infecções por Bactérias Gram-Negativas/microbiologia
Infecções por Bactérias Gram-Negativas/veterinária
Bactérias Gram-Positivas/fisiologia
Infecções por Bactérias Gram-Positivas/genética
Infecções por Bactérias Gram-Positivas/imunologia
Infecções por Bactérias Gram-Positivas/microbiologia
Infecções por Bactérias Gram-Positivas/veterinária
Lectinas Tipo C/química
Lectinas Tipo C/genética
Lectinas Tipo C/metabolismo
Subfamília D de Receptores Semelhantes a Lectina de Células NK/química
Subfamília D de Receptores Semelhantes a Lectina de Células NK/metabolismo
Alinhamento de Sequência/veterinária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Fish Proteins); 0 (Lectins, C-Type); 0 (NK Cell Lectin-Like Receptor Subfamily D)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170923
[Lr] Data última revisão:
170923
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


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[PMID]:27424220
[Au] Autor:Cipolla GA; Park JK; de Oliveira LA; Lobo-Alves SC; de Almeida RC; Farias TD; Lemos Dde S; Malheiros D; Lavker RM; Petzl-Erler ML
[Ad] Endereço:Department of Genetics, Federal University of Paraná, Curitiba, PR 81531-980, Brazil; CAPES Foundation, Ministry of Education of Brazil, Brasília, DF 70040-020, Brazil.
[Ti] Título:A 3'UTR polymorphism marks differential KLRG1 mRNA levels through disruption of a miR-584-5p binding site and associates with pemphigus foliaceus susceptibility.
[So] Source:Biochim Biophys Acta;1859(10):1306-13, 2016 10.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Genetic variations mapping to 3' untranslated regions (3'UTRs) may overlap with microRNA (miRNA) binding sites, therefore potentially interfering with translation inhibition or messenger RNA (mRNA) degradation. The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) located within the 3'UTRs of six candidate genes and predicted to interfere with miRNA ligation could account for disease-relevant differential mRNA levels. Focusing on pemphigus foliaceus (PF) - an autoimmune blistering skin condition with unique endemic patterns - we investigated whether nine 3'UTR SNPs from the CD1D, CTLA4, KLRD1, KLRG1, NKG7, and TNFSF13B genes differentially expressed in PF were disease-associated. The heterozygous genotype of the KLRG1 rs1805672 polymorphism was associated with increased predisposition to PF (A/G vs. A/A: P=0.038; OR=1.60), and a trend for augmented susceptibility was observed for carriers of the G allele (P=0.094; OR=1.44). In silico analyses suggested that rs1805672 G allele could disrupt binding of miR-584-5p, and indicated rs1805672 as an expression Quantitative Trait Locus (eQTL), with an effect on KLRG1 gene expression. Dual-luciferase assay showed that miR-584-5p mediated approximately 50% downregulation of the reporter gene's activity through the 3'UTR of KLRG1 harboring rs1805672 A allele (vs. miRNA-negative condition, P=0.006). This silencing relationship was lost after site-directed mutation to G allele (vs. miRNA-negative condition, P=0.391; vs. rs1805672 A allele, P=0.005). Collectively, these results suggest that a disease-associated SNP located within the 3'UTR of KLRG1 directly interferes with miR-584-5p binding, allowing for KLRG1 mRNA differential accumulation, which in turn may contribute to pathogenesis of autoimmune diseases, such as pemphigus.
[Mh] Termos MeSH primário: Regiões 3´ não Traduzidas
Predisposição Genética para Doença
Lectinas Tipo C/genética
MicroRNAs/genética
Pênfigo/genética
Polimorfismo de Nucleotídeo Único
Transativadores/genética
[Mh] Termos MeSH secundário: Alelos
Antígenos CD1d/genética
Antígenos CD1d/metabolismo
Fator Ativador de Células B/genética
Fator Ativador de Células B/metabolismo
Sequência de Bases
Sítios de Ligação
Antígeno CTLA-4/genética
Antígeno CTLA-4/metabolismo
Estudos de Casos e Controles
Análise Mutacional de DNA
Regulação da Expressão Gênica
Frequência do Gene
Haplótipos
Seres Humanos
Lectinas Tipo C/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
MicroRNAs/metabolismo
Mutação
Subfamília D de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília D de Receptores Semelhantes a Lectina de Células NK/metabolismo
Pênfigo/diagnóstico
Pênfigo/metabolismo
Pênfigo/patologia
Transativadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antigens, CD1d); 0 (B-Cell Activating Factor); 0 (CD1D protein, human); 0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (KLRD1 protein, human); 0 (KLRG1 protein, human); 0 (Lectins, C-Type); 0 (MIRN584 microRNA, human); 0 (Membrane Proteins); 0 (MicroRNAs); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (NKG7 protein, human); 0 (TNFSF13B protein, human); 0 (Trans-Activators)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160718
[St] Status:MEDLINE


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[PMID]:26850369
[Au] Autor:Verstrepen BE; Nieuwenhuis IG; Mooij P; Bogers WM; Boonstra A; Koopman G
[Ad] Endereço:Department of Virology, Biomedical Primate Research Centre, Rijswijk, the Netherlands.
[Ti] Título:Spontaneous and natural cytotoxicity receptor-mediated cytotoxicity are effector functions of distinct natural killer subsets in hepatitis C virus-infected chimpanzees.
[So] Source:Clin Exp Immunol;185(1):42-9, 2016 07.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In humans, CD16 and CD56 are used to identify functionally distinct natural killer (NK) subsets. Due to ubiquitous CD56 expression, this marker cannot be used to distinguish between NK cell subsets in chimpanzees. Therefore, functional analysis of distinct NK subsets during hepatitis C virus (HCV) infection has never been performed in these animals. In the present study an alternative strategy was used to identify four distinct NK subsets on the basis of the expression of CD16 and CD94. The expression of activating and inhibiting surface receptors showed that these subsets resemble human NK subsets. CD107 expression was used to determine degranulation of the different subsets in naive and HCV-infected chimpanzees. In HCV-infected chimpanzees increased spontaneous cytotoxicity was observed in CD94(high/dim) CD16(pos) and CD94(low) CD16(pos) subsets. By contrast, increased natural cytotoxicity receptor (NCR)- mediated degranulation after NKp30 and NKp44 triggering was demonstrated in the CD94(dim) CD16(neg) subset. Our findings suggest that spontaneous and NCR-mediated cytotoxicity are effector functions of distinct NK subsets in HCV-infected chimpanzees.
[Mh] Termos MeSH primário: Linhagem da Célula/imunologia
Citotoxicidade Imunológica
Hepacivirus/imunologia
Hepatite C/imunologia
Células Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Animais
Doenças dos Símios Antropoides
Degranulação Celular/efeitos dos fármacos
Citometria de Fluxo
Regulação da Expressão Gênica
Hepatite C/patologia
Hepatite C/virologia
Imunofenotipagem
Interleucina-2/farmacologia
Interleucinas/farmacologia
Células Matadoras Naturais/classificação
Células Matadoras Naturais/citologia
Células Matadoras Naturais/efeitos dos fármacos
Ativação Linfocitária/efeitos dos fármacos
Proteína 1 de Membrana Associada ao Lisossomo/genética
Proteína 1 de Membrana Associada ao Lisossomo/imunologia
Subfamília D de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília D de Receptores Semelhantes a Lectina de Células NK/imunologia
Receptor 2 Desencadeador da Citotoxicidade Natural/genética
Receptor 2 Desencadeador da Citotoxicidade Natural/imunologia
Receptor 3 Desencadeador da Citotoxicidade Natural/genética
Receptor 3 Desencadeador da Citotoxicidade Natural/imunologia
Pan troglodytes
Receptores de IgG/genética
Receptores de IgG/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-2); 0 (Interleukins); 0 (Lysosomal-Associated Membrane Protein 1); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Natural Cytotoxicity Triggering Receptor 2); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (Receptors, IgG); 0 (interleukin-21)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160207
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12774


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[PMID]:26828202
[Au] Autor:Davis ZB; Cogswell A; Scott H; Mertsching A; Boucau J; Wambua D; Le Gall S; Planelles V; Campbell KS; Barker E
[Ad] Endereço:Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois, United States of America.
[Ti] Título:A Conserved HIV-1-Derived Peptide Presented by HLA-E Renders Infected T-cells Highly Susceptible to Attack by NKG2A/CD94-Bearing Natural Killer Cells.
[So] Source:PLoS Pathog;12(2):e1005421, 2016 Feb.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Major histocompatibility class I (MHC-I)-specific inhibitory receptors on natural killer (NK) cells (iNKRs) tolerize mature NK cell responses toward normal cells. NK cells generate cytolytic responses to virus-infected or malignant target cells with altered or decreased MHC-I surface expression due to the loss of tolerizing ligands. The NKG2A/CD94 iNKR suppresses NK cell responses through recognition of the non-classical MHC-I, HLA-E. We used HIV-infected primary T-cells as targets in an in vitro cytolytic assay with autologous NK cells from healthy donors. In these experiments, primary NKG2A/CD94(+) NK cells surprisingly generated the most efficient responses toward HIV-infected T-cells, despite high HLA-E expression on the infected targets. Since certain MHC-I-presented peptides can alter recognition by iNKRs, we hypothesized that HIV-1-derived peptides presented by HLA-E on infected cells may block engagement with NKG2A/CD94, thereby engendering susceptibility to NKG2A/CD94(+) NK cells. We demonstrate that HLA-E is capable of presenting a highly conserved peptide from HIV-1 capsid (AISPRTLNA) that is not recognized by NKG2A/CD94. We further confirmed that HLA-C expressed on HIV-infected cells restricts attack by KIR2DL(+) CD56(dim) NK cells, in contrast to the efficient responses by CD56(bright) NK cells, which express predominantly NKG2A/CD94 and lack KIR2DLs. These findings are important since the use of NK cells was recently proposed to treat latently HIV-1-infected patients in combination with latency reversing agents. Our results provide a mechanistic basis to guide these future clinical studies, suggesting that ex vivo-expanded NKG2A/CD94(+) KIR2DL(-) NK cells may be uniquely beneficial.
[Mh] Termos MeSH primário: Infecções por HIV/imunologia
HIV-1/imunologia
Antígenos HLA-C/imunologia
Antígenos de Histocompatibilidade Classe I/imunologia
Células Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Seres Humanos
Subfamília D de Receptores Semelhantes a Lectina de Células NK/imunologia
Peptídeos/imunologia
Receptores de Células Matadoras Naturais/imunologia
Linfócitos T/imunologia
Linfócitos T/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (HLA-E antigen); 0 (Histocompatibility Antigens Class I); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Peptides); 0 (Receptors, Natural Killer Cell)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170527
[Lr] Data última revisão:
170527
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1005421


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[PMID]:26711740
[Au] Autor:Sasaki T; Kanaseki T; Shionoya Y; Tokita S; Miyamoto S; Saka E; Kochin V; Takasawa A; Hirohashi Y; Tamura Y; Miyazaki A; Torigoe T; Hiratsuka H; Sato N
[Ad] Endereço:Department of Pathology, Sapporo Medical University, Sapporo, Japan.
[Ti] Título:Microenvironmental stresses induce HLA-E/Qa-1 surface expression and thereby reduce CD8(+) T-cell recognition of stressed cells.
[So] Source:Eur J Immunol;46(4):929-40, 2016 Apr.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Hypoxia and glucose deprivation are often observed in the microenvironment surrounding solid tumors in vivo. However, how they interfere with MHC class I antigen processing and CD8(+) T-cell responses remains unclear. In this study, we analyzed the production of antigenic peptides presented by classical MHC class I in mice, and showed that it is quantitatively decreased in the cells exposed to either hypoxia or glucose deprivation. In addition, we unexpectedly found increased surface expression of HLA-E in human and Qa-1 in mouse tumor cells exposed to combined oxygen and glucose deprivation. The induced Qa-1 on the stressed tumor model interacted with an inhibitory NKG2/CD94 receptor on activated CD8(+) T cells and attenuated their specific response to the antigen. Our results thus suggest that microenvironmental stresses modulate not only classical but also nonclassical MHC class I presentation, and confer the stressed cells the capability to escape from the CD8(+) T-cell recognition.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Antígenos de Histocompatibilidade Classe I/biossíntese
Neoplasias/imunologia
Evasão Tumoral/imunologia
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno/imunologia
Hipóxia Celular/fisiologia
Linhagem Celular Tumoral
Glucose/deficiência
Antígenos de Histocompatibilidade Classe I/genética
Antígenos de Histocompatibilidade Classe I/imunologia
Seres Humanos
Células Matadoras Naturais/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Subfamília C de Receptores Semelhantes a Lectina de Células NK/imunologia
Subfamília D de Receptores Semelhantes a Lectina de Células NK/imunologia
Estresse Fisiológico/imunologia
Microambiente Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-E antigen); 0 (Histocompatibility Antigens Class I); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Q surface antigens); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160411
[Lr] Data última revisão:
160411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151230
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201545835


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[PMID]:26660880
[Au] Autor:Mazi E; Altunkaynak Z; Aydin I; Kocak I; Guven D; Turkmen AP; Yildiran A
[Ad] Endereço:Department of Pediatrics, School of Medicine, Ondokuz Mayis University, Samsun, Turkey.
[Ti] Título:Is parturition-timing machinery related to the number of inhibitor CD94/NKG2A positive uterine natural killer cells?
[So] Source:Arch Gynecol Obstet;294(2):261-5, 2016 Aug.
[Is] ISSN:1432-0711
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Prematurity is the most common cause of infant mortality and morbidity. To prevent this, the timing of parturition and its mechanisms should be understood. It is likely that inhibitor CD94/NKG2A positive decidual natural killer cells (uNK) provide for the continuation of pregnancy. Here, we aimed to evaluate whether CD94/NKG2A positive uNK cells are highest in elective cesarian section (C/S) (suggesting ongoing gestation), moderate in normal full-term birth, and lowest in pre-eclamptic parturition. METHODS: Of 48 pregnant women, 21 C/S, 16 normal, and 11 pre-eclamptic deliveries were included in this study. Five placentas in each group were assigned randomly. After staining, the volumetric analysis of the placental villi and villous blood vessels was performed via the Cavalieri principle. The CD94/NKG2A positive uNK cells were counted using the physical disector method. RESULTS: The gestation periods and birth weights of the pre-eclamptic deliveries were lower than those of the other two groups. Additionally, the villi and villous vascular volumes were lowest in the pre-eclamptic placentas. As proposed in our hypothesis, the inhibitor CD94/NKG2A positive uNK cells were the highest in the C/S, moderate in the normal, and lowest in the pre-eclamptic placentas. CONCLUSIONS: These data suggest that CD94/NKG2A positive uNK cells are related with the continuation of pregnancy, and that our human model could be used to search for parturition-timing machinery. We believe that CD94/NKG2A positive uNK cells are also related to the timing of birth.
[Mh] Termos MeSH primário: Células Matadoras Naturais/citologia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/metabolismo
Subfamília D de Receptores Semelhantes a Lectina de Células NK/metabolismo
[Mh] Termos MeSH secundário: Adulto
Decídua/citologia
Feminino
Seres Humanos
Gravidez
Receptores Imunológicos/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KLRD1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[St] Status:MEDLINE
[do] DOI:10.1007/s00404-015-3978-5


  10 / 504 MEDLINE  
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[PMID]:26453102
[Au] Autor:Iwaszko M; Swierkot J; Kolossa K; Jeka S; Wiland P; Bogunia-Kubik K
[Ad] Endereço:Laboratory of Clinical Immunogenetics and Pharmacogenetics, L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Weigla 12, 53-114 Wroclaw, Poland.
[Ti] Título:Influence of CD94 and NKG2A variants on susceptibility to rheumatoid arthritis and efficacy of anti-TNF treatment.
[So] Source:Joint Bone Spine;83(1):75-9, 2016 Jan.
[Is] ISSN:1778-7254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The present study aimed to investigate relationships between the CD94 and NKG2A gene polymorphisms and the risk of rheumatoid arthritis (RA) development as well as their association with the response to anti-TNF therapy. METHODS: A total of 284 patients with RA receiving anti-TNF therapy and 124 healthy subjects were enrolled to the study. Genotypings for CD94 (rs2302489) and NKG2A (rs7301582, rs2734440, rs2734414) polymorphisms were performed using a polymerase chain reaction (PCR) amplification employing LightSNiP assays (TIB-MolBiol, Berlin, Germany). Clinical response was evaluated at 12th and 24th week after initiation of the therapy according to the EULAR response criteria. RESULTS: The frequency of the CD94 AA genotype was significantly decreased in RA patients compared to controls (OR=0.44; P=0.016). The CD94 AA homozygotes were also more common among patients negative to anti-cyclic citrullinated peptide (anti-CCP) antibodies (OR=11.28; P=0.001) as compared to anti-CCP-positive patients and the presence of the CD94 allele A was associated with lack of anti-CCP antibodies (OR=5.00; P=0.0005). The CD94 rs2302489 TT genotype was over-represented in patients exhibiting worse EULAR response at 12th week (OR=3.33; P=0.017). Furthermore, the lack of response after 12 weeks was more frequent among patients carrying the NKG2A rs7301582C allele (OR=3.68; P=0.019) or the CC genotype (OR=3.58; P=0.035) in comparison to allele T or CT/TT genotypes, respectively. CONCLUSIONS: These results indicate that CD94 and NKG2A polymorphisms may contribute to genetic susceptibility to RA or affect the response to anti-TNF therapy in patients of Caucasian origin.
[Mh] Termos MeSH primário: Antirreumáticos/uso terapêutico
Artrite Reumatoide/tratamento farmacológico
Artrite Reumatoide/genética
Predisposição Genética para Doença
Subfamília C de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília D de Receptores Semelhantes a Lectina de Células NK/genética
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
Feminino
Genótipo
Glucocorticoides/uso terapêutico
Seres Humanos
Masculino
Metotrexato/uso terapêutico
Meia-Idade
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (Glucocorticoids); 0 (KLRC1 protein, human); 0 (KLRD1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (NK Cell Lectin-Like Receptor Subfamily D); 0 (Tumor Necrosis Factor-alpha); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160109
[Lr] Data última revisão:
160109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151011
[St] Status:MEDLINE



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