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Pesquisa : D12.776.543.750.705.871.300 [Categoria DeCS]
Referências encontradas : 9008 [refinar]
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  1 / 9008 MEDLINE  
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[PMID]:28743715
[Au] Autor:Tak T; Drylewicz J; Conemans L; de Boer RJ; Koenderman L; Borghans JAM; Tesselaar K
[Ad] Endereço:Department of Respiratory Medicine and.
[Ti] Título:Circulatory and maturation kinetics of human monocyte subsets in vivo.
[So] Source:Blood;130(12):1474-1477, 2017 09 21.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Monócitos/citologia
[Mh] Termos MeSH secundário: Asma/sangue
Diferenciação Celular
Senescência Celular
Replicação do DNA
Eosinofilia/sangue
Feminino
Proteínas Ligadas por GPI/análise
Homeostase
Seres Humanos
Imunofenotipagem
Cinética
Contagem de Leucócitos
Receptores de Lipopolissacarídeos/análise
Masculino
Modelos Biológicos
Monócitos/química
Monócitos/classificação
Receptores de IgG/análise
Valores de Referência
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (Lipopolysaccharide Receptors); 0 (Receptors, IgG)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-771261


  2 / 9008 MEDLINE  
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[PMID]:27773751
[Au] Autor:Pinkert S; Dieringer B; Diedrich S; Zeichhardt H; Kurreck J; Fechner H
[Ad] Endereço:Department of Applied Biochemistry, Institute of Biotechnology, Technische Universität Berlin, Berlin, Germany. Electronic address: sandra.pinkert@tu-berlin.de.
[Ti] Título:Soluble coxsackie- and adenovirus receptor (sCAR-Fc); a highly efficient compound against laboratory and clinical strains of coxsackie-B-virus.
[So] Source:Antiviral Res;136:1-8, 2016 12.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Coxsackie-B-viruses (CVB) cause a wide variety of diseases, ranging from mild syndromes to life-threatening conditions such as pancreatitis, myocarditis, meningitis and encephalitis. Especially newborns and young infants develop severe diseases and long-term sequelae may occur among survivors. Due to lack of specific antiviral therapy the current treatment of CVB infection is limited to symptomatic treatment. Here we analyzed the antiviral activity of a soluble receptor fusion protein, containing the extracellular part of the coxsackievirus and adenovirus receptor (CAR) fused to the constant domain of the human IgG - sCAR-Fc - against laboratory and clinical CVB strains. We found a high overall antiviral activity of sCAR-Fc against various prototypic laboratory strains of CVB, with an inhibition of viral replication up to 3 orders of magnitude (99.9%) at a concentration of 2.5 µg/ml. These include isolates that are not dependent on CAR for infection and isolates that are resistant against pleconaril, the currently most promising anti-CVB therapeutic. A complete inhibition was observed using higher concentration of sCAR-Fc. Further analysis of 23 clinical CVB isolates revealed overall high antiviral efficiency (up to 99.99%) of sCAR-Fc. In accordance with previous data, our results confirm the strong antiviral activity of sCAR-Fc against laboratory CVB strains and demonstrate for the first time that sCAR-Fc is also highly efficient at neutralizing clinical CVB isolates. Importantly, during the sCAR-Fc inhibition experiments, no naturally occurring resistant mutants were observed.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/química
Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/farmacologia
Enterovirus Humano B/efeitos dos fármacos
Imunoglobulina G/genética
[Mh] Termos MeSH secundário: Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/genética
Infecções por Coxsackievirus/tratamento farmacológico
Infecções por Coxsackievirus/virologia
Células HeLa
Seres Humanos
Imunoglobulina G/farmacologia
Receptores de IgG
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/farmacologia
Solubilidade
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Coxsackie and Adenovirus Receptor-Like Membrane Protein); 0 (Immunoglobulin G); 0 (Receptors, IgG); 0 (Recombinant Fusion Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  3 / 9008 MEDLINE  
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[PMID]:29190833
[Au] Autor:Horvei KD; Pedersen HL; Fismen S; Thiyagarajan D; Schneider A; Rekvig OP; Winkler TH; Seredkina N
[Ad] Endereço:RNA and Molecular Pathology Research Group, Department of Medical Biology, Faculty of Health Sciences, UIT-The Arctic University of Norway, Tromsø, Norway.
[Ti] Título:Lupus nephritis progression in FcγRIIB-/-yaa mice is associated with early development of glomerular electron dense deposits and loss of renal DNase I in severe disease.
[So] Source:PLoS One;12(11):e0188863, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FcγRIIB-/-yaa mice develop severe lupus glomerulonephritis due to lack of an inhibitory immune cell receptor combined with a Y-chromosome linked autoimmune accelerator mutation. In the present study, we have investigated nephritis development and progression in FcγRIIB-/-yaa mice to find shared features with NZB/NZW F1 lupus prone mice and human disease. We sacrificed 25 male FcγRIIB-/-yaa mice at various disease stages, and grouped them according to activity and chronicity indices for lupus nephritis. Glomerular morphology and localization of electron dense deposits containing IgG were further determined by immune electron microscopy. Renal DNase I and pro-inflammatory cytokine mRNA levels were measured by real-time quantitative PCR. DNase I protein levels was assessed by immunohistochemistry and zymography. Our results demonstrate early development of electron dense deposits containing IgG in FcγRIIB-/-yaa mice, before detectable levels of serum anti-dsDNA antibodies. Similar to NZB/NZW F1, electron dense deposits in FcγRIIB-/-yaa progressed from being confined to the mesangium in the early stage of lupus nephritis to be present also in capillary glomerular basement membranes. In the advanced stage of lupus nephritis, renal DNase I was lost on both transcriptional and protein levels, which has previously been shown in NZB/NZW F1 mice and in human disease. Although lupus nephritis appears on different genetic backgrounds, our findings suggest similar processes when comparing different murine models and human lupus nephritis.
[Mh] Termos MeSH primário: Desoxirribonuclease I/metabolismo
Glomérulos Renais/patologia
Nefrite Lúpica/patologia
Receptores de IgG/genética
[Mh] Termos MeSH secundário: Animais
Progressão da Doença
Imunoglobulina G/metabolismo
Glomérulos Renais/enzimologia
Glomérulos Renais/metabolismo
Túbulos Renais/metabolismo
Nefrite Lúpica/metabolismo
Masculino
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Receptor 7 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fcgr2b protein, mouse); 0 (Immunoglobulin G); 0 (Membrane Glycoproteins); 0 (Receptors, IgG); 0 (Tlr7 protein, mouse); 0 (Toll-Like Receptor 7); EC 3.1.21.1 (Deoxyribonuclease I)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188863


  4 / 9008 MEDLINE  
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[PMID]:28982863
[Au] Autor:Pham DH; Kim JS; Kim SK; Shin DJ; Uong NT; Hyun H; Yoon MS; Kang SJ; Ryu YJ; Cho JS; Yoon JH; Lee JS; Cho D; Lee SH; Park MH
[Ad] Endereço:Department of Biomedical Sciences, Chonnam National University Medical School, Gwangju, Republic of Korea.
[Ti] Título:Effects of ADAM10 and ADAM17 Inhibitors on Natural Killer Cell Expansion and Antibody-dependent Cellular Cytotoxicity Against Breast Cancer Cells .
[So] Source:Anticancer Res;37(10):5507-5513, 2017 10.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The inhibition of a disintegrin and metalloproteinase (ADAM) has the potential to become a novel approach for natural killer (NK) cell-based cancer immunotherapy. Thus, the aim of this study was to investigate the influence of ADAM10 and ADAM17 inhibitors on expanded NK cell to enhance antibody-dependent cellular cytotoxicity (ADCC) in breast cancer cell lines. MATERIALS AND METHODS: NK cells were expanded in medium supplemented with an ADAM10 or ADAM17 inhibitor to prevent the shedding of soluble CD16/FcγRIII. The expression level of CD16 and production of interferon-gamma (IFN-γ) was detected by flow cytometry using specific antibodies. ADCC activity of expanded NK cells was estimated in trastuzumab treated breast cancer cell lines such as MCF-7, MDA-MB-231, SKBR3, and BT-474 cells. RESULTS: The ADAM17 inhibitor increased the purity of expanded NK cells to 90% after 14 days at 5 and 10 µM in vitro (p=0.043). However, the expansion rate of NK cells was decreased at 10 µM of the ADAM 17 inhibitor (p=0.043). Inhibition of ADAM10 suppressed the expansion of NK cells, although the NK purity was increased at 1 µM of the inhibitor. The expression of CD16 was significantly increased at 1 and 5 µM of the ADAM17 inhibitor (p=0.046, 0.028, respectively) during the culturing period. Inhibition of ADAM10 reduced the expression of CD16 on NK cells. The cytotoxic activity of the ADAM17 inhibitor treated NK cells against MCF-7 (p=0.039) and BT-474 (p=0.027) cells was significantly elevated. The ADCC activity of NK cells treated with 5 µM of ADAM17 inhibitor was significantly increased against SKBR-3 and BT-474 (p=0.027). Inhibition of ADAM17 increased the production of IFN-γ in expanded NK cells. CONCLUSION: The inhibition of ADAM17 enhanced the purity of expanded NK cells and the ADCC activity of these cells against trastuzumab treated breast cancer cell lines.
[Mh] Termos MeSH primário: Proteína ADAM10/antagonistas & inibidores
Proteína ADAM17/antagonistas & inibidores
Secretases da Proteína Precursora do Amiloide/antagonistas & inibidores
Citotoxicidade Celular Dependente de Anticorpos/efeitos dos fármacos
Antineoplásicos/farmacologia
Neoplasias da Mama/tratamento farmacológico
Proliferação Celular/efeitos dos fármacos
Células Matadoras Naturais/efeitos dos fármacos
Ativação Linfocitária/efeitos dos fármacos
Proteínas de Membrana/antagonistas & inibidores
Inibidores de Proteases/farmacologia
[Mh] Termos MeSH secundário: Proteína ADAM10/metabolismo
Proteína ADAM17/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Neoplasias da Mama/enzimologia
Neoplasias da Mama/imunologia
Neoplasias da Mama/patologia
Técnicas de Cocultura
Relação Dose-Resposta a Droga
Feminino
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Interferon gama/metabolismo
Células Matadoras Naturais/enzimologia
Células Matadoras Naturais/imunologia
Células MCF-7
Proteínas de Membrana/metabolismo
Receptores de IgG/metabolismo
Fatores de Tempo
Trastuzumab/farmacologia
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (IFNG protein, human); 0 (Membrane Proteins); 0 (Protease Inhibitors); 0 (Receptors, IgG); 82115-62-6 (Interferon-gamma); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (ADAM10 protein, human); EC 3.4.24.86 (ADAM17 Protein); EC 3.4.24.86 (ADAM17 protein, human); P188ANX8CK (Trastuzumab)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


  5 / 9008 MEDLINE  
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[PMID]:28891817
[Au] Autor:Nishi H; Furuhashi K; Cullere X; Saggu G; Miller MJ; Chen Y; Rosetti F; Hamilton SL; Yang L; Pittman SP; Liao J; Herter JM; Berry JC; DeAngelo DJ; Zhu C; Tsokos GC; Mayadas TN
[Ad] Endereço:Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases.
[So] Source:J Clin Invest;127(10):3810-3826, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The kidney glomerular capillaries are frequent sites of immune complex deposition and subsequent neutrophil accumulation in post-infectious and rapidly progressive glomerulonephritis. However, the mechanisms of neutrophil recruitment remain enigmatic, and there is no targeted therapeutic to avert this proximal event in glomerular inflammation. The uniquely human activating Fc receptor FcγRIIA promotes glomerular neutrophil accumulation and damage in anti-glomerular basement membrane-induced (anti-GBM-induced) glomerulonephritis when expressed on murine neutrophils. Here, we found that neutrophils are directly captured by immobilized IgG antibodies under physiological flow conditions in vitro through FcγRIIA-dependent, Abl/Src tyrosine kinase-mediated F-actin polymerization. Biophysical measurements showed that the lifetime of FcγRIIA-IgG bonds increased under mechanical force in an F-actin-dependent manner, which could enable the capture of neutrophils under physiological flow. Kidney intravital microscopy revealed that circulating neutrophils, which were similar in diameter to glomerular capillaries, abruptly arrested following anti-GBM antibody deposition via neutrophil FcγRIIA and Abl/Src kinases. Accordingly, inhibition of Abl/Src with bosutinib reduced FcγRIIA-mediated glomerular neutrophil accumulation and renal injury in experimental, crescentic anti-GBM nephritis. These data identify a pathway of neutrophil recruitment within glomerular capillaries following IgG deposition that may be targeted by bosutinib to avert glomerular injury.
[Mh] Termos MeSH primário: Compostos de Anilina/farmacologia
Glomerulonefrite/imunologia
Imunoglobulina G/imunologia
Glomérulos Renais/imunologia
Neutrófilos/imunologia
Nitrilos/farmacologia
Quinolinas/farmacologia
Receptores de IgG/imunologia
[Mh] Termos MeSH secundário: Animais
Capilares/imunologia
Capilares/patologia
Glomerulonefrite/genética
Glomerulonefrite/patologia
Células HL-60
Seres Humanos
Glomérulos Renais/patologia
Camundongos
Camundongos Knockout
Neutrófilos/patologia
Proteínas Proto-Oncogênicas c-abl/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-abl/genética
Proteínas Proto-Oncogênicas c-abl/imunologia
Receptores de IgG/genética
Quinases da Família src/antagonistas & inibidores
Quinases da Família src/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (FCGR2A protein, human); 0 (Immunoglobulin G); 0 (Nitriles); 0 (Quinolines); 0 (Receptors, IgG); 5018V4AEZ0 (bosutinib); EC 2.7.10.2 (Proto-Oncogene Proteins c-abl); EC 2.7.10.2 (src-Family Kinases)
[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


  6 / 9008 MEDLINE  
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[PMID]:28886140
[Au] Autor:Kwon YC; Kim JJ; Yun SW; Yu JJ; Yoon KL; Lee KY; Kil HR; Kim GB; Han MK; Song MS; Lee HD; Ha KS; Sohn S; Ebata R; Hamada H; Suzuki H; Ito K; Onouchi Y; Hong YM; Jang GY; Lee JK; Korean Kawasaki Disease Genetics Consortium
[Ad] Endereço:Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea.
[Ti] Título:Male-specific association of the FCGR2A His167Arg polymorphism with Kawasaki disease.
[So] Source:PLoS One;12(9):e0184248, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kawasaki disease (KD) is an acute systemic vasculitis that can potentially cause coronary artery aneurysms in some children. KD occurs approximately 1.5 times more frequently in males than in females. To identify sex-specific genetic variants that are involved in KD pathogenesis in children, we performed a sex-stratified genome-wide association study (GWAS), using the Illumina HumanOmni1-Quad BeadChip data (249 cases and 1,000 controls) and a replication study for the 34 sex-specific candidate SNPs in an independent sample set (671 cases and 3,553 controls). Male-specific associations were detected in three common variants: rs1801274 in FCGR2A [odds ratio (OR) = 1.40, P = 9.31 × 10-5], rs12516652 in SEMA6A (OR = 1.87, P = 3.12 × 10-4), and rs5771303 near IL17REL (OR = 1.57, P = 2.53 × 10-5). The male-specific association of FCGR2A, but not SEMA6A and IL17REL, was also replicated in a Japanese population (OR = 1.74, P = 1.04 × 10-4 in males vs. OR = 1.22, P = 0.191 in females). In a meta-analysis with 1,461 cases and 5,302 controls, a very strong association of KD with the nonsynonymous SNP rs1801274 (p.His167Arg, previously assigned as p.His131Arg) in FCGR2A was confirmed in males (OR = 1.48, P = 1.43 × 10-7), but not in the females (OR = 1.17, P = 0.055). The present study demonstrates that p.His167Arg, a KD-associated FCGR2A variant, acts as a susceptibility gene in males only. Overall, the gender differences associated with FCGR2A in KD provide a new insight into KD susceptibility.
[Mh] Termos MeSH primário: Substituição de Aminoácidos
Códon
Predisposição Genética para Doença
Síndrome de Linfonodos Mucocutâneos/genética
Polimorfismo de Nucleotídeo Único
Receptores de IgG/genética
[Mh] Termos MeSH secundário: Alelos
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
Feminino
Estudos de Associação Genética
Genótipo
Seres Humanos
Japão
Masculino
Razão de Chances
Receptores de Interleucina-17/genética
República da Coreia
Semaforinas/genética
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon); 0 (FCGR2A protein, human); 0 (IL17REL protein, human); 0 (Receptors, IgG); 0 (Receptors, Interleukin-17); 0 (SEMA6A protein, human); 0 (Semaphorins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184248


  7 / 9008 MEDLINE  
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[PMID]:28880939
[Au] Autor:Lin JS; Jeon JS; Fan Q; Wong HN; Palmer MB; Holzman LB
[Ad] Endereço:Division of Internal Medicine, Department of Emergency Medicine, Section of Nephrology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
[Ti] Título:ARF6 mediates nephrin tyrosine phosphorylation-induced podocyte cellular dynamics.
[So] Source:PLoS One;12(9):e0184575, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ADP-ribosylation factor 6 (ARF6) is a small GTPase necessary for regulating cellular structure, motility, and vesicle trafficking. In several cellular systems, ARF6 was shown to regulate actin dynamics in coordination with Rac1, a Rho small GTPase. We examined the function of ARF6 in the kidney podocyte because Rac1 was implicated in kidney diseases involving this cell. We found that ARF6 expression was enriched in human podocytes and that it modulated podocyte cytoskeletal dynamics through a functional interaction with nephrin, an intercellular junction protein necessary for podocyte injury-induced signaling requiring activation by tyrosine phosphorylation of its cytoplasmic domain. ARF6 was necessary for nephrin activation-induced ruffling and focal adhesion turnover, possibly by altering Rac1 activity. In podocyte-specific Arf6 (ARF6_PodKO) knockout mice, ARF6 deficiency did not result in a spontaneous kidney developmental phenotype or proteinuria after aging. However, ARF6_PodKO mice exhibited distinct phenotypes in two in vivo glomerular injury models. In the protamine sulfate perfusion model, which induced acute podocyte effacement, ARF6_PodKO mice were protected from podocyte effacement. In the nephrotoxic serum nephritis model, which induced immune-complex mediated injury, ARF6_PodKO mice exhibited aggravated proteinuria. Together, these observations suggest that while ARF6 is necessary for nephrin tyrosine phosphorylation-induced cytoskeletal dynamics in cultured podocytes, ARF6 has pleotropic podocyte roles in vivo, where glomerular injury-specific mechanisms might activate distinct signaling pathways that dictate whether ARF6 activity is beneficial or deleterious for maintaining the integrity of the glomerular filtration barrier.
[Mh] Termos MeSH primário: Fatores de Ribosilação do ADP/metabolismo
Nefrite/metabolismo
[Mh] Termos MeSH secundário: Fatores de Ribosilação do ADP/genética
Animais
Feminino
Seres Humanos
Rim/metabolismo
Rim/patologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Nefrite/genética
Podócitos/metabolismo
Receptores de IgG/genética
Receptores de IgG/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Receptors, IgG); 0 (nephrin); EC 3.6.5.2 (ADP-Ribosylation Factors); EC 3.6.5.2 (ADP-ribosylation factor 6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184575


  8 / 9008 MEDLINE  
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[PMID]:28837583
[Au] Autor:An X; Sendra VG; Liadi I; Ramesh B; Romain G; Haymaker C; Martinez-Paniagua M; Lu Y; Radvanyi LG; Roysam B; Varadarajan N
[Ad] Endereço:Department of Chemical and Biomolecular Engineering, University of Houston, Houston, Texas, United States of America.
[Ti] Título:Single-cell profiling of dynamic cytokine secretion and the phenotype of immune cells.
[So] Source:PLoS One;12(8):e0181904, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are a highly heterogeneous population of innate lymphocytes that constitute our first line of defense against several types of tumors and microbial infections. Understanding the heterogeneity of these lymphocytes requires the ability to integrate their underlying phenotype with dynamic functional behaviors. We have developed and validated a single-cell methodology that integrates cellular phenotyping and dynamic cytokine secretion based on nanowell arrays and bead-based molecular biosensors. We demonstrate the robust passivation of the polydimethylsiloxane (PDMS)-based nanowells arrays with polyethylene glycol (PEG) and validated our assay by comparison to enzyme-linked immunospot (ELISPOT) assays. We used numerical simulations to optimize the molecular density of antibodies on the surface of the beads as a function of the capture efficiency of cytokines within an open-well system. Analysis of hundreds of individual human peripheral blood NK cells profiled ex vivo revealed that CD56dimCD16+ NK cells are immediate secretors of interferon gamma (IFN-γ) upon activation by phorbol 12-myristate 13-acetate (PMA) and ionomycin (< 3 h), and that there was no evidence of cooperation between NK cells leading to either synergistic activation or faster IFN-γ secretion. Furthermore, we observed that both the amount and rate of IFN-γ secretion from individual NK cells were donor-dependent. Collectively, these results establish our methodology as an investigational tool for combining phenotyping and real-time protein secretion of individual cells in a high-throughput manner.
[Mh] Termos MeSH primário: Citocinas/secreção
Imunofenotipagem
Células Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Antígeno CD56/imunologia
Dimetilpolisiloxanos
Ensaio de Imunoadsorção Enzimática
Proteínas Ligadas por GPI/imunologia
Seres Humanos
Células Matadoras Naturais/efeitos dos fármacos
Receptores de IgG/imunologia
Análise de Célula Única
Acetato de Tetradecanoilforbol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD56 Antigen); 0 (Cytokines); 0 (Dimethylpolysiloxanes); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (NCAM1 protein, human); 0 (Receptors, IgG); 63148-62-9 (baysilon); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[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:170825
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181904


  9 / 9008 MEDLINE  
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[PMID]:28829829
[Au] Autor:Neuser J; Galuppo P; Fraccarollo D; Willig J; Kempf T; Berliner D; Bauersachs J; Widder JD
[Ad] Endereço:Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
[Ti] Título:Intermediate CD14++CD16+ monocytes decline after transcatheter aortic valve replacement and correlate with functional capacity and left ventricular systolic function.
[So] Source:PLoS One;12(8):e0183670, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Transcatheter aortic valve replacement (TAVR) is the method of choice for patients with severe aortic valve stenosis, who are ineligible or at high risk for surgery. Though TAVR leads to a significant reduction in mortality, a notable amount of patients are re-hospitalized early after TAVR. Parameters or biomarkers predicting outcome are therefore needed to identify patients who benefit most. Specific monocyte subsets have been associated with cardiovascular diseases and were shown to possess prognostic value. METHODS: Peripheral blood was drawn before and after transfemoral TAVR with the self-expanding CoreValve, Boston Lotus or the balloon-expanding Edwards Sapien prosthesis. Classical (CD14++CD16-), intermediate (CD14++CD16+) and non-classical (CD14+CD16++) monocyte subsets were determined by flow cytometry. Transthoracic echocardiography was performed before, early after as well as 3 months after the TAVR procedure. RESULTS: No significant differences in the absolute monocyte counts were found after TAVR. A significant decline in the intermediate monocyte population was though observed early after TAVR (pre 4.01±0.38%, post 2.803±0.34%, p≤0.05). Creatinine levels stayed stable after TAVR procedure and intermediate monocytes were associated with worse renal function. Monocyte decline was not related to changes in CRP-, noradrenaline, cortisol or aldosterone-levels. The amount of intermediate monocytes correlated with worse cardiac function and predicted the possibility to reach an improvement in NYHA functional class at 3 months after TAVR. CONCLUSIONS: A significant decline of intermediate monocytes occurs shortly after TAVR. High levels of intermediate monocytes were associated with worse cardiac function and predicted poor functional capacity, hinting at a possible prognostic value.
[Mh] Termos MeSH primário: Receptores de Lipopolissacarídeos/imunologia
Monócitos/imunologia
Receptores de IgG/imunologia
Sístole
Substituição da Valva Aórtica Transcateter
Função Ventricular Esquerda
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharide Receptors); 0 (Receptors, IgG)
[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:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183670


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[PMID]:28814603
[Au] Autor:Brandsma AM; Ten Broeke T; van Dueren den Hollander E; Caniels TG; Kardol-Hoefnagel T; Kuball J; Leusen JHW
[Ad] Endereço:Laboratory of Translational Immunology, University Medical Center Utrecht, 3584 CX Utrecht, the Netherlands.
[Ti] Título:Single Nucleotide Polymorphisms of the High Affinity IgG Receptor FcγRI Reduce Immune Complex Binding and Downstream Effector Functions.
[So] Source:J Immunol;199(7):2432-2439, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Binding of IgG Abs to FcγRs on immune cells induces FcγR cross-linking that leads to cellular effector functions, such as phagocytosis, Ab-dependent cellular cytotoxicity, and cytokine release. However, polymorphisms in low affinity FcγRs have been associated with altered avidity toward IgG, thereby substantially impacting clinical outcomes of multimodular therapy when targeting cancer or autoimmune diseases with mAbs as well as the frequency and severity of autoimmune diseases. In this context, we investigated the consequences of three nonsynonymous single nucleotide polymorphisms (SNPs) for the high affinity receptor for IgG, FcγRI. Only SNP V39I, located in the extracellular domain of FcγRI, reduces immune-complex binding of FcγRI whereas monomeric IgG binding is unaffected. This leads to reduced FcγRI effector functions, including Fc receptor γ-chain signaling and intracellular calcium mobilization. SNPs I301M and I338T, located in the transmembrane or intracellular domain, respectively, have no influence on monomeric IgG or immune complex binding, but FcRγ signaling is decreased for both SNPs, especially for I338T. We also found that the frequency of these SNPs in a cohort of healthy Dutch individuals is very low within the population. To our knowledge, this study addresses for the first time the biological consequences of SNPs in the high affinity FcγR, and reveals reduction in several FcγRI functions, which have the potential to alter efficacy of therapeutic Abs.
[Mh] Termos MeSH primário: Complexo Antígeno-Anticorpo/metabolismo
Imunoglobulina G/metabolismo
Polimorfismo de Nucleotídeo Único
Receptores de IgG/genética
[Mh] Termos MeSH secundário: Animais
Genótipo
Seres Humanos
Imunoglobulina G/genética
Camundongos
Fagocitose
Ligação Proteica
Receptores de IgG/deficiência
Receptores de IgG/imunologia
Receptores de IgG/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigen-Antibody Complex); 0 (FCGR1A protein, human); 0 (Fcgr1 protein, mouse); 0 (Immunoglobulin G); 0 (Receptors, IgG)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601929



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