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[PMID]:29372577
[Au] Autor:Mansouri F; Heydarzadeh R; Yousefi S
[Ad] Endereço:Department of Genetics and Immunology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
[Ti] Título:The association of interferon-gamma, interleukin-4 and interleukin-17 single-nucleotide polymorphisms with susceptibility to tuberculosis.
[So] Source:APMIS;126(3):227-233, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Susceptibility to tuberculosis and progression of the disease depend on interactions between the bacterial agent, host immune system, and environmental and genetic factors. In this case-controlled study, we aimed to determine the role of single-nucleotide polymorphisms of interferon-gamma, interleukin-4 and interleukin-17 in susceptibility to tuberculosis. Genomic DNA was extracted from peripheral blood samples of patients and controls. The association of single-nucleotide polymorphisms in interleukin-4 (-590C/T), interleukin-17 (-152A/G) and interferon-gamma (+874T/A) was investigated by polymerase chain reaction (PCR)-restriction fragment length polymorphism and amplification refractory mutation system-PCR. A total of 76 tuberculosis patients and 119 healthy individuals were included in this study. The interferon-gamma (+874T/A) TA genotype was significantly associated with susceptibility to tuberculosis in patients compared to controls (OR = 1.76; 95%CI = 0.84-3.71; p = 0.007), while the interferon-gamma (+874T/A) TT genotype (OR = 0.51; 95%CI = 0.19-1.36; p = 0.007) had protective effects against tuberculosis and was related to a low risk of tuberculosis development. The difference between allelic and genotypic frequencies of interleukin-4 (-590C/T) between patients and controls was not significant (p = 0.46). Multivariate logistic regression analysis revealed that the interleukin-17 (-152A/G) AG genotype (OR = 2.27; 95%CI = 1.19-4.34; p = 0.03) and AA genotype (OR = 1.03; 95%CI = 0.43-2.44; p = 0.03) were significantly different between patients and controls. In conclusion, single-nucleotide mutations in different cytokine genes may have protective effects or increase the risk of tuberculosis.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Interferon gama/genética
Interleucina-17/genética
Interleucina-4/genética
Tuberculose Pulmonar/genética
[Mh] Termos MeSH secundário: Adulto
Alelos
Estudos de Casos e Controles
DNA/genética
Feminino
Frequência do Gene/genética
Genótipo
Seres Humanos
Masculino
Meia-Idade
Mycobacterium tuberculosis/imunologia
Técnicas de Amplificação de Ácido Nucleico
Polimorfismo de Fragmento de Restrição
Polimorfismo de Nucleotídeo Único/genética
Tuberculose Pulmonar/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (IL4 protein, human); 0 (Interleukin-17); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma); 9007-49-2 (DNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12810


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[PMID]:29458538
[Au] Autor:Ma J; Yu L; Song B; Yu Y; Zhang S; Wei Y; Wu Z; Yao D; Yu W; Zhu Z; Cui Y
[Ad] Endereço:1​College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing 163319, PR China.
[Ti] Título:The double adjuvants LTB and CpG significantly enhanced the immuno-protective effects of recombinant GIT derived from Staphylococcus aureus and Streptococcus in mice.
[So] Source:J Med Microbiol;67(3):432-440, 2018 Mar.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: In this study, we prepared GapC1-150-IsdB126-361-TRAP (GIT) proteins plus heat-labile enterotoxin B (LTB) as an intra-molecular adjuvant, together with CpG to further enhance its immunogenicity. METHODOLOGY: Initially, the target genes were acquired and inserted into pET-32a (+) vectors to express LTB-GIT protein. LTB-GIT expression was confirmed by Western blotting and its immunocompetence was estimated through ELISA. Further, we immunized BALB/c mice with the LTB-GIT plus CpG adjuvant. After the second immunization, the antigen-specific CD4 cell responses for IFN-γ, IL-2, IL-4 and IL-10 were monitored by intracellular cytokine staining (ICS) assay. After the third immunization, the level of IgG antibodies in the serum from immunized groups was assessed by ELISA, and the protective immune response was appraised by Staphylococcus aureus and Streptococcus dysgalactiae challenge. RESULTS: The ELISA results showed that the OD450nm value of the LTB-GIT group was significantly higher than that of the BSA group. The group immunized with LTB-GIT plus CpG exhibited significantly stronger CD4 T cell responses for IFN-γ, IL-2, IL-4 and IL-10 compared to the group immunized with LTB-GIT, GIT alone orLTB-GIT plus CpG. In addition, the group immunized with LTB-GIT plus CpG generated the highest level of IgG antibodies against GIT among all of the groups, and our results also showed that LTB-GIT plus CpG markedly improved the survival percentage of mice compared to other groups. CONCLUSION: We confirmed that the novel double adjuvants, LTB and CpG, are able to significantly improve GIT-induced immune responses. This formula could be a promising strategy for enhancing the immune efficacy of multi-subunit vaccines against Staphylococcus aureus and streptococcal infection.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos
Toxinas Bacterianas/imunologia
Vacinas Bacterianas/imunologia
Enterotoxinas/imunologia
Oligodesoxirribonucleotídeos/imunologia
Staphylococcus aureus/imunologia
Streptococcus/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antibacterianos/sangue
Antígenos de Bactérias/imunologia
Proteínas de Bactérias/imunologia
Toxinas Bacterianas/administração & dosagem
Toxinas Bacterianas/genética
Linfócitos T CD4-Positivos
Enterotoxinas/administração & dosagem
Enterotoxinas/genética
Feminino
Interferon gama/imunologia
Interleucina-10/imunologia
Interleucina-2/imunologia
Interleucina-4/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Oligodesoxirribonucleotídeos/genética
Proteínas Recombinantes/genética
Proteínas Recombinantes/imunologia
Infecções Estafilocócicas/imunologia
Staphylococcus aureus/química
Infecções Estreptocócicas/imunologia
Streptococcus/química
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antibodies, Bacterial); 0 (Antigens, Bacterial); 0 (Bacterial Proteins); 0 (Bacterial Toxins); 0 (Bacterial Vaccines); 0 (CPG-oligonucleotide); 0 (Enterotoxins); 0 (IL10 protein, mouse); 0 (Interleukin-2); 0 (Oligodeoxyribonucleotides); 0 (Recombinant Proteins); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000666


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[PMID]:29185091
[Au] Autor:Kolben T; Jeschke U; Reimer T; Karsten N; Schmoeckel E; Semmlinger A; Mahner S; Harbeck N; Kolben TM
[Ad] Endereço:Department of Obstetrics and Gynecology, University Hospital, Ludwig-Maximilians-University Munich, Marchioninistr. 15, 81377, Munich, Germany. Thomas.Kolben@med.uni-muenchen.de.
[Ti] Título:Induction of apoptosis in breast cancer cells in vitro by Fas ligand reverse signaling.
[So] Source:J Cancer Res Clin Oncol;144(2):249-256, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The Fas-antigen is a cell surface receptor that transduces apoptotic signals into cells. The purpose of this study was to evaluate FasL expression in breast cancer and to elucidate the role of its signaling in different breast cancer cell lines. METHODS: T47D and MCF7 cells were used and cultured in Dulbecco's modified Eagle's medium. FasL translocation to the membrane was achieved by culturing the cells in the presence of human interferon-γ (IFNγ). Translocation was detected by immunofluorescence. The ability of a Fas:Fc fusion protein to trigger apoptosis in these cells was investigated by cell death detection ELISA. After incubation with IFNγ for 4 h and 18 h, apoptosis was assessed in response to treatment with Fas:Fc. RESULTS: Immunofluorescence revealed that the used cell lines were positive for FasL which was increased and changed to more membrane-bound FasL expression after IFNγ stimulation. After stimulation with 50 IU/ml IFNγ, Fas:Fc significantly increased MCF7 apoptosis (1.39 ± 0.06-fold, p = 0.0004) after 18 h. After stimulation with 100 IU/ml, Fas:Fc significantly increased apoptosis both after 4 h (1.49 ± 0.15-fold, p = 0.018) and 18 h (1.30 ± 0.06-fold, p = 0.013). In T47D cells this effect was seen after 4 h of stimulation with 50 IU/ml and addition of Fas:Fc (1.6 ± 0.08-fold, p = 0.03). CONCLUSION: Membrane-bound FasL expression could be induced by IFNγ in a breast cancer cell model. More importantly, in the presence of IFNγ the Fas:Fc fusion protein was able to transmit pro-apoptotic signals to T47D and MCF7 cells, significantly inducing apoptosis. The current findings support further in vivo studies regarding FasL activation as a potential target for therapeutic intervention in breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Proteína Ligante Fas/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Neoplasias da Mama/tratamento farmacológico
Ensaio de Imunoadsorção Enzimática
Proteína Ligante Fas/genética
Feminino
Imunofluorescência
Seres Humanos
Fragmentos Fc das Imunoglobulinas/genética
Interferon gama/farmacologia
Células MCF-7
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (IFNG protein, human); 0 (Immunoglobulin Fc Fragments); 0 (Recombinant Fusion Proteins); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2551-y


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[PMID]:28467275
[Au] Autor:Dos Santos PF; Mansur DS
[Ad] Endereço:Departament of Microbiology, Immunology and Parasitology, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina , Santa Catarina, Brazil .
[Ti] Título:Beyond ISGlylation: Functions of Free Intracellular and Extracellular ISG15.
[So] Source:J Interferon Cytokine Res;37(6):246-253, 2017 Jun.
[Is] ISSN:1557-7465
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ISG15 is a ubiquitin-like type I IFN-stimulated protein of 15 kDa and is one of the most prominently expressed proteins in viral infections. ISG15 is widely known to be involved in a process called ISGylation, where it binds to over 150 targets from a variety of classes of proteins including central immune signaling pathways such as those mediated by NFκB, JNK, and IRF-3. However, ISG15 also exists in a free form that can act intra- or extracellularly. In vitro and in vivo evidences suggest that free ISG15 play different roles in several cellular processes, from cancer and defense against viral infections to activation of immune cells such as lymphocytes, monocytes, and NK cells. This review discusses the roles of free intracellular and secreted ISG15 approaching questions yet to be answered about the mechanism of action of this protein.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Citocinas/imunologia
Interferon gama/imunologia
Transdução de Sinais/imunologia
Ubiquitinas/imunologia
Viroses/imunologia
[Mh] Termos MeSH secundário: Infecções Bacterianas/genética
Infecções Bacterianas/microbiologia
Citocinas/genética
Regulação da Expressão Gênica
Seres Humanos
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Interferon gama/genética
Monócitos/imunologia
Monócitos/microbiologia
Monócitos/virologia
Neutrófilos/imunologia
Neutrófilos/microbiologia
Neutrófilos/virologia
Linfócitos T/imunologia
Linfócitos T/microbiologia
Linfócitos T/virologia
Ubiquitinas/genética
Viroses/genética
Viroses/virologia
eIF-2 Quinase/genética
eIF-2 Quinase/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Interferon Type I); 0 (Ubiquitins); 60267-61-0 (ISG15 protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/jir.2016.0103


  5 / 62981 MEDLINE  
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[PMID]:28460461
[Au] Autor:Nilofar Danishmalik S; Lee SH; Sin JI
[Ad] Endereço:BK21 Plus Graduate Program and Department of Microbiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon-do 200-701, Korea.
[Ti] Título:Tumor regression is mediated via the induction of HER263-71- specific CD8+ CTL activity in a 4T1.2/HER2 tumor model: no involvement of CD80 in tumor control.
[So] Source:Oncotarget;8(16):26771-26788, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the CT26/HER2 and 4T1.2/HER2 tumor models, CT26/HER2 cells form tumors that continue to grow, whereas 4T1.2/HER2 cells form tumors that eventually regress. Here, we investigated the differences in the behaviors of these two cell lines. When immune cells from 4T1.2/HER2 tumor-bearing animals were stimulated with HER2 class I peptides, they displayed a 2-fold increase in IFN-γ levels, in response to the peptides, HER263-71 and HER2342-350. In contrast, extremely high levels of antigen-non-specific IFN-γ production were observed with immune cells and sera from CT26/HER2 tumor-bearing mice. However, IFN-γ had no effect on tumor progression in the CT26/HER2 model, as determined by an IFN-γ knockout assay. 4T1.2/HER2 tumor-bearing mice displayed CTL activity in response to HER263-71 but not to HER2342-350, whereas no such induction was observed in CT26/HER2 tumor-bearing mice. When 4T1.2/HER2 cell-challenged mice were depleted of CD8+ T cells, they lost their tumor-regressing activity, suggesting an antitumor role of HER263-71-specific CD8+ CTLs in the control of this tumor type. CT26/HER2 cells also expressed CD80. However, CD80-transfected 4T1.2/HER2 and CD80-non-expressing CT26/HER2 cells failed to alter their tumorigenicity, suggesting no role of CD80 in tumor control. Despite increased levels of myeloid-derived suppressor cells in the tumor, they were not associated with tumor progression in the CT26/HER2 model, as determined by a cell depletion assay. Overall, these data show that, contrary to CT26/HER2 tumors, 4T1.2/HER2 tumors regress via the induction of HER263-71-specific CD8+ CTLs and that CD80 is not associated with the regression of these tumors.
[Mh] Termos MeSH primário: Neoplasias/imunologia
Neoplasias/metabolismo
Receptor ErbB-2/imunologia
Especificidade do Receptor de Antígeno de Linfócitos T/imunologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/imunologia
Biomarcadores
Linhagem Celular Tumoral
Desoxicitidina/análogos & derivados
Desoxicitidina/farmacologia
Modelos Animais de Doenças
Feminino
Imunoglobulina G/imunologia
Interferon gama/genética
Interferon gama/metabolismo
Camundongos
Camundongos Knockout
Neoplasias/patologia
Subpopulações de Linfócitos T/efeitos dos fármacos
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Citotóxicos/efeitos dos fármacos
Células Th1/imunologia
Células Th1/metabolismo
Carga Tumoral/efeitos dos fármacos
Carga Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (Immunoglobulin G); 0W860991D6 (Deoxycytidine); 82115-62-6 (Interferon-gamma); B76N6SBZ8R (gemcitabine); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15816


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[PMID]:29421440
[Au] Autor:Wen A; Qu XH; Zhang KN; Leng EL; Ren Y; Wu XM
[Ad] Endereço:Department of Neurology, People's Hospital of Jiangxi Province, Nanchang, Jiangxi Province, China; Institution of Neurology, People's Hospital of Jiangxi Province, Nanchang, Jiangxi Province, China.
[Ti] Título:Evaluation of interferon-gamma release assays in extrasanguinous body fluids for diagnosing tuberculosis: A systematic review and meta-analysis.
[So] Source:Life Sci;197:140-146, 2018 Mar 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: In this study, we conducted a meta-analysis to systematically compare the diagnostic accuracy of IGRAs performed for extrasanguinous body fluids with that performed for blood in the diagnosis of TB. MAIN METHODS: Multiple English and Chinese databases were searched up to November 2017. Studies that complied with the guidelines for the Quality Assessment of Diagnostic Accuracy Studies and used QuantiFERON-TB Gold In-Tube and/or T-SPOT.TB (ELISPOT) assays on both blood and extrasanguinous body fluids were included. Statistical analysis was performed using Stata 12.0 software. Since publication bias is a concern in the meta-analysis of diagnostic studies, we tested for this using Begg's funnel plots. KEY FINDING: Among the 1332 articles searched from the databases, 24 articles met the inclusion criteria, which included 1040 samples in the patient group and 1044 samples in the control group. For extrasanguinous body fluids, the pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and summary receiver operating characteristic (SROC) area under the curve (AUC) were 87% (95% CI: 0.81-0.91), 89% (95% CI: 0.84-0.93), 8.22 (95% CI 5.38-12.56), 0.15 (95% CI: 0.10-0.21), 44.92 (95% CI: 25.61-78.81), and 0.94 (95% CI: 0.92-0.96), respectively. For peripheral blood, these values were 83% (95% CI: 0.79-0.87), 74% (95% CI: 0.68-0.79), 3.17 (95% CI 2.63-3.84), 0.23 (95% CI: 0.19-0.29), 12.99 (95% CI: 10.19-16.57), and 0.86 (95% CI: 0.82-0.89), respectively. SIGNIFICANCE: IGRAs performed on extrasanguinous body fluids exhibited a better diagnostic accuracy compared with IGRAs performed on peripheral blood for diagnosing TB.
[Mh] Termos MeSH primário: Líquidos Corporais/metabolismo
Interferon gama/metabolismo
Tuberculose/diagnóstico
Tuberculose/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (IFNG protein, human); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE


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[PMID]:28463086
[Au] Autor:Mann EH; Ho TR; Pfeffer PE; Matthews NC; Chevretton E; Mudway I; Kelly FJ; Hawrylowicz CM
[Ad] Endereço:1 MRC and Asthma-UK Centre for Allergic Mechanisms in Asthma, and.
[Ti] Título:Vitamin D Counteracts an IL-23-Dependent IL-17A IFN-γ Response Driven by Urban Particulate Matter.
[So] Source:Am J Respir Cell Mol Biol;57(3):355-366, 2017 09.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health. This is hypothesized to be due in part to regulation of IL-17A, which UPM is reported to promote. Here, we used a myeloid dendritic cell (DC)-memory CD4 T cell co-culture system to characterize UPM-driven IL-17A cells, investigate the mechanism by which UPM-primed DCs promote this phenotype, and address evidence for cross-regulation by vitamin D. CD1c myeloid DCs were cultured overnight with or without a reference source of UPM and/or active vitamin D (1,25[OH] D ) before they were co-cultured with autologous memory CD4 T cells. Supernatants were harvested for cytokine analysis on Day 5 of co-culture, and intracellular cytokine staining was performed on Day 7. UPM-primed DCs increased the proportion of memory CD4 T cells expressing the T helper 17 cell (Th17)-associated cytokines IL-17A, IL-17F, and IL-22, as well as IFN-γ, granulocyte-macrophage colony-stimulating factor, and granzyme B. Notably, a large proportion of the UPM-driven IL-17A cells co-expressed these cytokines, but not IL-10, indicative of a proinflammatory Th17 profile. UPM-treated DCs expressed elevated levels of il23 mRNA and increased secretion of IL-23p40. Neutralization of IL-23 in culture reduced the frequency of IL-17A IFN-γ cells without affecting cell proliferation. 1,25(OH) D counteracted the UPM-driven DC maturation and inhibited the frequency of IL-17A IFN-γ cells, most prominently when DCs were co-treated with the corticosteroid dexamethasone, while maintaining antiinflammatory IL-10 synthesis. These data indicate that UPM might promote an inflammatory milieu in part by inducing an IL-23-driven proinflammatory Th17 response. Restoring vitamin D sufficiency may counteract these UPM-driven effects without obliterating important homeostatic immune functions.
[Mh] Termos MeSH primário: Cidades
Interferon gama/metabolismo
Interleucina-17/metabolismo
Interleucina-23/metabolismo
Material Particulado/toxicidade
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Calcitriol/farmacologia
Diferenciação Celular/efeitos dos fármacos
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Dexametasona/farmacologia
Seres Humanos
Células Mieloides/efeitos dos fármacos
Células Mieloides/metabolismo
Fenótipo
Células Th17/imunologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Particulate Matter); 1406-16-2 (Vitamin D); 7S5I7G3JQL (Dexamethasone); 82115-62-6 (Interferon-gamma); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0409OC


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[PMID]:28459437
[Au] Autor:Toussaint M; Jackson DJ; Swieboda D; Guedán A; Tsourouktsoglou TD; Ching YM; Radermecker C; Makrinioti H; Aniscenko J; Bartlett NW; Edwards MR; Solari R; Farnir F; Papayannopoulos V; Bureau F; Marichal T; Johnston SL
[Ad] Endereço:Airway Disease Infection Section, National Heart and Lung Institute (NHLI), Imperial College London, London, UK.
[Ti] Título:Host DNA released by NETosis promotes rhinovirus-induced type-2 allergic asthma exacerbation.
[So] Source:Nat Med;23(6):681-691, 2017 06.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Respiratory viral infections represent the most common cause of allergic asthma exacerbations. Amplification of the type-2 immune response is strongly implicated in asthma exacerbation, but how virus infection boosts type-2 responses is poorly understood. We report a significant correlation between the release of host double-stranded DNA (dsDNA) following rhinovirus infection and the exacerbation of type-2 allergic inflammation in humans. In a mouse model of allergic airway hypersensitivity, we show that rhinovirus infection triggers dsDNA release associated with the formation of neutrophil extracellular traps (NETs), known as NETosis. We further demonstrate that inhibiting NETosis by blocking neutrophil elastase or by degrading NETs with DNase protects mice from type-2 immunopathology. Furthermore, the injection of mouse genomic DNA alone is sufficient to recapitulate many features of rhinovirus-induced type-2 immune responses and asthma pathology. Thus, NETosis and its associated extracellular dsDNA contribute to the pathogenesis and may represent potential therapeutic targets of rhinovirus-induced asthma exacerbations.
[Mh] Termos MeSH primário: Asma/imunologia
Citocinas/imunologia
DNA/imunologia
Armadilhas Extracelulares/imunologia
Infecções por Picornaviridae/imunologia
Hipersensibilidade Respiratória/imunologia
Infecções Respiratórias/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Adulto
Animais
Estudos de Casos e Controles
Dermatophagoides farinae/imunologia
Modelos Animais de Doenças
Feminino
Seres Humanos
Interferon gama/imunologia
Interleucina-13/imunologia
Interleucina-4/imunologia
Interleucina-5/imunologia
Masculino
Camundongos
Meia-Idade
Rhinovirus
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-13); 0 (Interleukin-5); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma); 9007-49-2 (DNA)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4332


  9 / 62981 MEDLINE  
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[PMID]:29324751
[Au] Autor:Echebli N; Tchitchek N; Dupuy S; Bruel T; Peireira Bittencourt Passaes C; Bosquet N; Le Grand R; Bourgeois C; Favier B; Cheynier R; Lambotte O; Vaslin B
[Ad] Endereço:CEA, Université Paris Sud, INSERM U1184, Immunology of Viral Infections and Autoimmune Diseases (IMVA), IDMIT Department / IBFJ, Fontenay-aux-Roses, France.
[Ti] Título:Stage-specific IFN-induced and IFN gene expression reveal convergence of type I and type II IFN and highlight their role in both acute and chronic stage of pathogenic SIV infection.
[So] Source:PLoS One;13(1):e0190334, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interferons (IFNs) play a major role in controlling viral infections including HIV/SIV infections. Persistent up-regulation of interferon stimulated genes (ISGs) is associated with chronic immune activation and progression in SIV/HIV infections, but the respective contribution of different IFNs is unclear. We analyzed the expression of IFN genes and ISGs in tissues of SIV infected macaques to understand the respective roles of type I and type II IFNs. Both IFN types were induced in lymph nodes during early stage of primary infection and to some extent in rectal biopsies but not in PBMCs. Induction of Type II IFN expression persisted during the chronic phase, in contrast to undetectable induction of type I IFN expression. Global gene expression analysis with a major focus on ISGs revealed that at both acute and chronic infection phases most differentially expressed ISGs were inducible by both type I and type II IFNs and displayed the highest increases, indicating strong convergence and synergy between type I and type II IFNs. The analysis of functional signatures of ISG expression revealed temporal changes in IFN expression patterns identifying phase-specific ISGs. These results suggest that IFN-γ strongly contribute to shape ISG upregulation in addition to type I IFN.
[Mh] Termos MeSH primário: Expressão Gênica
Interferon Tipo I/genética
Interferon gama/genética
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Doença Crônica
Macaca fascicularis
Vírus da Imunodeficiência Símia/imunologia
Vírus da Imunodeficiência Símia/fisiologia
Transcriptoma
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interferon Type I); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190334


  10 / 62981 MEDLINE  
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[PMID]:29304133
[Au] Autor:Eberle KC; Venn-Watson SK; Jensen ED; LaBresh J; Sullivan Y; Kakach L; Sacco RE
[Ad] Endereço:Ruminant Diseases and Immunology Research Unit, National Animal Disease Center, Agricultural Research Service, United States Department of Agriculture, Ames, IA, United States of America.
[Ti] Título:Development and testing of species-specific ELISA assays to measure IFN-γ and TNF-α in bottlenose dolphins (Tursiops truncatus).
[So] Source:PLoS One;13(1):e0190786, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Monitoring the immune status of cetaceans is important for a variety of health conditions. Assays to quantify cytokines, especially pro-inflammatory cytokines, could be employed, in addition to currently available diagnostic assays, to screen for alterations in the health status of an animal. Though a number of immunological assays are readily available for humans and mice, specific assays for many veterinary species, including cetaceans such as bottlenose dolphins (Tursiops truncatus), are more limited. Herein, we describe the development of IFN-gamma (IFN-γ) and TNF-alpha (TNF-α) enzyme-linked immunosorbent assays (ELISAs) specific to bottlenose dolphins. Utilizing these assays, we monitored the immune status of bottlenose dolphins from a managed population over a period of eleven months. The ELISA assays developed for bottlenose dolphins were used to measure IFN-γ and TNF-α in serum or in culture supernatants from peripheral blood mononuclear cells (PBMCs) stimulated with varying concentrations of mitogens concanavalin A (ConA) or phytohemagglutinin (PHA). Induction of TNF-α in PBMC cultures was consistently highest with 1 µg/mL ConA, while 1 µg/mL PHA induced the highest secretion of IFN-γ. Serum levels of TNF-α and IFN-γ remained relatively constant for each animal over the time period examined. CBC and plasma chemistry variables measured concurrently in the bottlenose dolphins were then examined as independent predictors of cytokine levels. We found these clinical variables were more likely to predict linear changes in serum IFN-γ and TNF-α levels compared to concentrations of these cytokines in mitogen-stimulated PBMC culture supernatants. Cytokine assays developed will be of substantial benefit in monitoring bottlenose dolphin health as an adjunct to currently available diagnostic tests.
[Mh] Termos MeSH primário: Golfinho Nariz-de-Garrafa/sangue
Ensaio de Imunoadsorção Enzimática/métodos
Interferon gama/sangue
Fator de Necrose Tumoral alfa/sangue
[Mh] Termos MeSH secundário: Animais
Meios de Cultura
Feminino
Leucócitos Mononucleares/metabolismo
Masculino
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190786



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