Base de dados : MEDLINE
Pesquisa : B04.280.650.160.650.200 [Categoria DeCS]
Referências encontradas : 351 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 36 ir para página                         

  1 / 351 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28453414
[Au] Autor:Dolega P; Szulc-Dabrowska L; Bossowska M; Mielcarska M; Nowak Z; Toka FN
[Ad] Endereço:1 Division of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences , Warsaw, Poland .
[Ti] Título:Innate Immune Gene Transcript Level Associated with the Infection of Macrophages with Ectromelia Virus in Two Different Mouse Strains.
[So] Source:Viral Immunol;30(5):315-329, 2017 06.
[Is] ISSN:1557-8976
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Poxviruses have evolved numerous mechanisms to avoid the immune response of the infected host, and many of these mechanisms have not been fully described. Here, we studied the transcriptional response of innate immune genes in BALB/c and C57BL/6 peritoneal macrophages following infection with the Moscow strain of ectromelia virus (ECTV-Mos) with the aim of delineating innate immune genes that contribute to the difference between susceptibility and resistance to lethal infection. We show a generalized downregulation of many genes in four categories (toll-like receptor signaling, NOD-like receptor signaling, RIG-I-like receptor signaling, and type I interferon signaling) of antiviral innate immune receptors, downstream signaling pathways, and responsive components. Two important observations were made. First, 14 innate antiviral genes were differentially expressed with fold change upregulation of two and above occurring in C57BL/6 mice, known to be resistant to ECTV-Mos infection, whereas the same genes were downregulated in BALB/c mice with fold change of two and below. Second, the cathepsin group of genes was downregulated in both strains of mice but with profound fold changes of 17, 38, and 62 downregulation for CtsL, CtsB, and CtsS, respectively, in C57BL/6 mice. We show that a poxvirus profoundly downregulates both the mRNA and protein expression of these three cathepsins and this change appears to support virus replication. Based on these data we propose that the variations in gene expression observed may contribute to the difference in resistance/susceptibility between BALB/c and C57BL/6 mice to lethal infection by ECTV-Mos.
[Mh] Termos MeSH primário: Resistência à Doença
Vírus da Ectromelia/imunologia
Ectromelia Infecciosa/imunologia
Perfilação da Expressão Gênica
Imunidade Inata
Macrófagos Peritoneais/imunologia
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1089/vim.2016.0173


  2 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28628829
[Au] Autor:Frey TR; Lehmann MH; Ryan CM; Pizzorno MC; Sutter G; Hersperger AR
[Ad] Endereço:Department of Biology, Albright College, Reading, PA, USA.
[Ti] Título:Ectromelia virus accumulates less double-stranded RNA compared to vaccinia virus in BS-C-1 cells.
[So] Source:Virology;509:98-111, 2017 Sep.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most orthopoxviruses, including vaccinia virus (VACV), contain genes in the E3L and K3L families. The protein products of these genes have been shown to combat PKR, a host defense pathway. Interestingly, ectromelia virus (ECTV) contains an E3L ortholog but does not possess an intact K3L gene. Here, we gained insight into how ECTV can still efficiently evade PKR despite lacking K3L. Relative to VACV, we found that ECTV-infected BS-C-1 cells accumulated considerably less double-stranded (ds) RNA, which was due to lower mRNA levels and less transcriptional read-through of some genes by ECTV. The abundance of dsRNA in VACV-infected cells, detected using a monoclonal antibody, was able to activate the RNase L pathway at late time points post-infection. Historically, the study of transcription by orthopoxviruses has largely focused on VACV as a model. Our data suggest that there could be more to learn by studying other members of this genus.
[Mh] Termos MeSH primário: Vírus da Ectromelia/fisiologia
RNA de Cadeia Dupla/metabolismo
Vírus Vaccinia/fisiologia
Replicação Viral
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cercopithecus aethiops
Células Epiteliais/virologia
Evasão da Resposta Imune
RNA de Cadeia Dupla/imunologia
RNA Mensageiro/metabolismo
RNA Viral/metabolismo
Transcrição Genética
eIF-2 Quinase/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Double-Stranded); 0 (RNA, Messenger); 0 (RNA, Viral); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


  3 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28604814
[Au] Autor:Szulc-Dabrowska L; Struzik J; Ostrowska A; Guzera M; Toka FN; Bossowska-Nowicka M; Gierynska MM; Winnicka A; Nowak Z; Niemialtowski MG
[Ad] Endereço:Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences-SGGW, Warsaw, Poland.
[Ti] Título:Functional paralysis of GM-CSF-derived bone marrow cells productively infected with ectromelia virus.
[So] Source:PLoS One;12(6):e0179166, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ectromelia virus (ECTV) is an orthopoxvirus responsible for mousepox, a lethal disease of certain strains of mice that is similar to smallpox in humans, caused by variola virus (VARV). ECTV, similar to VARV, exhibits a narrow host range and has co-evolved with its natural host. Consequently, ECTV employs sophisticated and host-specific strategies to control the immune cells that are important for induction of antiviral immune response. In the present study we investigated the influence of ECTV infection on immune functions of murine GM-CSF-derived bone marrow cells (GM-BM), comprised of conventional dendritic cells (cDCs) and macrophages. Our results showed for the first time that ECTV is able to replicate productively in GM-BM and severely impaired their innate and adaptive immune functions. Infected GM-BM exhibited dramatic changes in morphology and increased apoptosis during the late stages of infection. Moreover, GM-BM cells were unable to uptake and process antigen, reach full maturity and mount a proinflammatory response. Inhibition of cytokine/chemokine response may result from the alteration of nuclear translocation of NF-κB, IRF3 and IRF7 transcription factors and down-regulation of many genes involved in TLR, RLR, NLR and type I IFN signaling pathways. Consequently, GM-BM show inability to stimulate proliferation of purified allogeneic CD4+ T cells in a primary mixed leukocyte reaction (MLR). Taken together, our data clearly indicate that ECTV induces immunosuppressive mechanisms in GM-BM leading to their functional paralysis, thus compromising their ability to initiate downstream T-cell activation events.
[Mh] Termos MeSH primário: Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/virologia
Vírus da Ectromelia/fisiologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/farmacologia
[Mh] Termos MeSH secundário: Animais
Antígenos/imunologia
Apoptose/efeitos dos fármacos
Células da Medula Óssea/metabolismo
Linhagem Celular
Células Cultivadas
Citocinas/metabolismo
Endocitose/efeitos dos fármacos
Endocitose/imunologia
Imunofenotipagem
Interferon Tipo I/metabolismo
Leucócitos/imunologia
Leucócitos/metabolismo
Leucócitos/virologia
Ativação Linfocitária/imunologia
Masculino
Camundongos
Transdução de Sinais
Linfócitos T/imunologia
Linfócitos T/metabolismo
Receptor 4 Toll-Like/agonistas
Receptor 4 Toll-Like/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Cytokines); 0 (Interferon Type I); 0 (Toll-Like Receptor 4); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179166


  4 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28282449
[Au] Autor:Aguirre de Cárcer D; Hernáez B; Rastrojo A; Alcamí A
[Ad] Endereço:Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid (UAM), Madrid, Spain.
[Ti] Título:Infection with diverse immune-modulating poxviruses elicits different compositional shifts in the mouse gut microbiome.
[So] Source:PLoS One;12(3):e0173697, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is often not possible to demonstrate causality within the context of gut microbiota dysbiosis-linked diseases. Thus, we need a better understanding of the mechanisms whereby an altered host immunophysiology shapes its resident microbiota. In this regard, immune-modulating poxvirus strains and mutants could differentially alter gut mucosal immunity in the context of a natural immune response, providing a controlled natural in vivo setting to deepen our understanding of the immune determinants of microbiome composition. This study represents a proof-of-concept that the use of an existing collection of different immune-modulating poxviruses may represent an innovative tool in gut microbiome research. To this end, 16S rRNA amplicon sequencing and RNAseq transcriptome profiling were employed as proxies for microbiota composition and gut immunophysiological status in the analysis of caecal samples from control mice and mice infected with various poxvirus types. Our results show that different poxvirus species and mutants elicit different shifts in the mice mucosa-associated microbiota and, in some instances, significant concomitant shifts in gut transcriptome profiles, thus providing an initial validation to the proposed model.
[Mh] Termos MeSH primário: Microbioma Gastrointestinal/fisiologia
Infecções por Poxviridae/imunologia
Poxviridae/patogenicidade
[Mh] Termos MeSH secundário: Animais
Vírus da Ectromelia/genética
Vírus da Ectromelia/patogenicidade
Feminino
Microbioma Gastrointestinal/imunologia
Interações Hospedeiro-Patógeno/imunologia
Camundongos Endogâmicos BALB C
Mutação
Poxviridae/genética
Poxviridae/imunologia
Infecções por Poxviridae/microbiologia
Infecções por Poxviridae/fisiopatologia
RNA Ribossômico 16S
Vírus Vaccinia/genética
Vírus Vaccinia/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Ribosomal, 16S)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173697


  5 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27898336
[Au] Autor:Reynolds SE; Earl PL; Minai M; Moore I; Moss B
[Ad] Endereço:Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Fairleigh Dickinson University, 285 Madison Avenue, Madison, NJ 07940, USA.
[Ti] Título:A homolog of the variola virus B22 membrane protein contributes to ectromelia virus pathogenicity in the mouse footpad model.
[So] Source:Virology;501:107-114, 2017 Jan 15.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most poxviruses encode a homolog of a ~200,000-kDa membrane protein originally identified in variola virus. We investigated the importance of the ectromelia virus (ECTV) homolog C15 in a natural infection model. In cultured mouse cells, the replication of a mutant virus with stop codons near the N-terminus (ECTV-C15Stop) was indistinguishable from a control virus (ECTV-C15Rev). However, for a range of doses injected into the footpads of BALB/c mice there was less mortality with the mutant. Similar virus loads were present at the site of infection with mutant or control virus whereas there was less ECTV-C15Stop in popliteal and inguinal lymph nodes, spleen and liver indicating decreased virus spread and replication. The latter results were supported by immunohistochemical analyses. Decreased spread was evidently due to immune modulatory activity of C15, rather than to an intrinsic viral function, as the survival of infected mice depended on CD4+ and CD8+ T cells.
[Mh] Termos MeSH primário: Vírus da Ectromelia/metabolismo
Vírus da Ectromelia/patogenicidade
Ectromelia Infecciosa/metabolismo
Ectromelia Infecciosa/virologia
Proteínas de Membrana/metabolismo
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Vírus da Ectromelia/genética
Ectromelia Infecciosa/genética
Ectromelia Infecciosa/patologia
Feminino
Seres Humanos
Fígado/patologia
Fígado/virologia
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos BALB C
Baço/patologia
Baço/virologia
Vírus da Varíola/genética
Vírus da Varíola/metabolismo
Proteínas Virais/genética
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Viral Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE


  6 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27455306
[Au] Autor:Garver J; Weber L; Vela EM; Anderson M; Warren R; Merchlinsky M; Houchens C; Rogers JV
[Ad] Endereço:Battelle Biomedical Research Center, West Jefferson, OH 43162, USA. garverj@battelle.org.
[Ti] Título:Ectromelia Virus Disease Characterization in the BALB/c Mouse: A Surrogate Model for Assessment of Smallpox Medical Countermeasures.
[So] Source:Viruses;8(7), 2016 Jul 22.
[Is] ISSN:1999-4915
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:In 2007, the United States- Food and Drug Administration (FDA) issued guidance concerning animal models for testing the efficacy of medical countermeasures against variola virus (VARV), the etiologic agent for smallpox. Ectromelia virus (ECTV) is naturally-occurring and responsible for severe mortality and morbidity as a result of mousepox disease in the murine model, displaying similarities to variola infection in humans. Due to the increased need of acceptable surrogate animal models for poxvirus disease, we have characterized ECTV infection in the BALB/c mouse. Mice were inoculated intranasally with a high lethal dose (125 PFU) of ECTV, resulting in complete mortality 10 days after infection. Decreases in weight and temperature from baseline were observed eight to nine days following infection. Viral titers via quantitative polymerase chain reaction (qPCR) and plaque assay were first observed in the blood at 4.5 days post-infection and in tissue (spleen and liver) at 3.5 days post-infection. Adverse clinical signs of disease were first observed four and five days post-infection, with severe signs occurring on day 7. Pathological changes consistent with ECTV infection were first observed five days after infection. Examination of data obtained from these parameters suggests the ECTV BALB/c model is suitable for potential use in medical countermeasures (MCMs) development and efficacy testing.
[Mh] Termos MeSH primário: Vírus da Ectromelia/isolamento & purificação
Ectromelia Infecciosa/patologia
Doenças dos Roedores/patologia
[Mh] Termos MeSH secundário: Administração Intranasal
Experimentação Animal
Animais
Temperatura Corporal
Peso Corporal
Ectromelia Infecciosa/virologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Reação em Cadeia da Polimerase em Tempo Real
Doenças dos Roedores/virologia
Análise de Sobrevida
Fatores de Tempo
Carga Viral
Ensaio de Placa Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160726
[St] Status:MEDLINE


  7 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27169394
[Au] Autor:Szulc-Dabrowska L; Gregorczyk KP; Struzik J; Boratynska-Jasinska A; Szczepanowska J; Wyzewski Z; Toka FN; Gierynska M; Ostrowska A; Niemialtowski MG
[Ad] Endereço:Division of Immunology, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences-SGGW, Warsaw, Poland.
[Ti] Título:Remodeling of the fibroblast cytoskeletal architecture during the replication cycle of Ectromelia virus: A morphological in vitro study in a murine cell line.
[So] Source:Cytoskeleton (Hoboken);73(8):396-417, 2016 Aug.
[Is] ISSN:1949-3592
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ectromelia virus (ECTV, the causative agent of mousepox), which represents the same genus as variola virus (VARV, the agent responsible for smallpox in humans), has served for years as a model virus for studying mechanisms of poxvirus-induced disease. Despite increasing knowledge on the interaction between ECTV and its natural host-the mouse-surprisingly, still little is known about the cell biology of ECTV infection. Because pathogen interaction with the cytoskeleton is still a growing area of research in the virus-host cell interplay, the aim of the present study was to evaluate the consequences of ECTV infection on the cytoskeleton in a murine fibroblast cell line. The viral effect on the cytoskeleton was reflected by changes in migration of the cells and rearrangement of the architecture of tubulin, vimentin, and actin filaments. The virus-induced cytoskeletal rearrangements observed in these studies contributed to the efficient cell-to-cell spread of infection, which is an important feature of ECTV virulence. Additionally, during later stages of infection L929 cells produced two main types of actin-based cellular protrusions: short (actin tails and "dendrites") and long (cytoplasmic corridors). Due to diversity of filopodial extensions induced by the virus, we suggest that ECTV represents a valuable new model for studying processes and pathways that regulate the formation of cytoskeleton-based cellular structures. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Citoesqueleto/metabolismo
Vírus da Ectromelia/crescimento & desenvolvimento
Fibroblastos/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Vírus da Ectromelia/metabolismo
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160513
[St] Status:MEDLINE
[do] DOI:10.1002/cm.21308


  8 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26791861
[Au] Autor:Sigal LJ
[Ad] Endereço:Thomas Jefferson University, Department of Microbiology and Immunology, Philadelphia, Pennsylvania, USA. Electronic address: Luis.Sigal@Jefferson.edu.
[Ti] Título:The Pathogenesis and Immunobiology of Mousepox.
[So] Source:Adv Immunol;129:251-76, 2016.
[Is] ISSN:1557-8445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ectromelia virus is a mouse-specific orthopoxvirus that, following footpad infection or natural transmission, causes mousepox in most strains of mice, while a few strains, such as C57BL/6, are resistant to the disease but not to the infection. Mousepox is an acute, systemic, highly lethal disease of remarkable semblance to smallpox, caused by the human-specific variola virus. Starting in 1929 with its discovery by Marchal, work with ECTV has provided essential information for our current understanding on how viruses spread lympho-hematogenously, the genetic control of antiviral resistance, the role of different components of the innate and adaptive immune system in the control of primary and secondary infections with acute viruses, and how the mechanisms of immune evasion deployed by the virus affect virulence in vivo. Here, I review the literature on the pathogenesis and immunobiology of ECTV infection in vivo.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Resistência à Doença/imunologia
Vírus da Ectromelia/patogenicidade
Ectromelia Infecciosa/imunologia
Varíola/imunologia
Vírus Vaccinia/imunologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Vírus da Ectromelia/imunologia
Ectromelia Infecciosa/prevenção & controle
Ectromelia Infecciosa/virologia
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Vacinação
Proteínas Virais/imunologia
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160122
[St] Status:MEDLINE


  9 / 351 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26780774
[Au] Autor:Bien K; Sobanska Z; Sokolowska J; Baska P; Nowak Z; Winnicka A; Krzyzowska M
[Ad] Endereço:Department of Regenerative Medicine, Military Institute of Hygiene and Epidemiology, Kozielska 4, 01-163, Warsaw, Poland.
[Ti] Título:A lack of Fas/FasL signalling leads to disturbances in the antiviral response during ectromelia virus infection.
[So] Source:Arch Virol;161(4):913-28, 2016 Apr.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Ectromelia virus (ECTV) is an orthopoxvirus (OPV) that causes mousepox, the murine equivalent of human smallpox. Fas receptor-Fas ligand (FasL) signaling is involved in apoptosis of immune cells and virus-specific cytotoxicity. The Fas/FasL pathway also plays an important role in controlling the local inflammatory response during ECTV infection. Here, the immune response to the ECTV Moscow strain was examined in Fas (-) (lpr), FasL (-) (gld) and C57BL6 wild-type mice. During ECTV-MOS infection, Fas- and FasL mice showed increased viral titers, decreased total numbers of NK cells, CD4(+) and CD8(+) T cells followed by decreased percentages of IFN-γ expressing NK cells, CD4(+) and CD8(+) T cells in spleens and lymph nodes. At day 7 of ECTV-MOS infection, Fas- and FasL-deficient mice had the highest regulatory T cell (Treg) counts in spleen and lymph nodes in contrast to wild-type mice. Furthermore, at days 7 and 10 of the infection, we observed significantly higher numbers of PD-L1-expressing dendritic cells in Fas (-) and FasL (-) mice in comparison to wild-type mice. Experiments in co-cultures of CD4(+) T cells and bone-marrow-derived dendritic cells showed that the lack of bilateral Fas-FasL signalling led to expansion of Tregs. In conclusion, our results demonstrate that during ECTV infection, Fas/FasL can regulate development of tolerogenic DCs and Tregs, leading to an ineffective immune response.
[Mh] Termos MeSH primário: Vírus da Ectromelia
Ectromelia Infecciosa/metabolismo
Proteína Ligante Fas/metabolismo
Receptor fas/metabolismo
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea
Linfócitos T CD4-Positivos/fisiologia
Linfócitos T CD4-Positivos/virologia
Linhagem Celular
Cercopithecus aethiops
Técnicas de Cocultura
Células Dendríticas/fisiologia
Células Dendríticas/virologia
Ectromelia Infecciosa/imunologia
Ectromelia Infecciosa/virologia
Proteína Ligante Fas/genética
Regulação da Expressão Gênica
Células Matadoras Naturais
Linfonodos
Masculino
Camundongos
Transdução de Sinais
Baço
Fatores de Tempo
Receptor fas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fas Ligand Protein); 0 (Fas protein, mouse); 0 (Fasl protein, mouse); 0 (fas Receptor)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-015-2746-y


  10 / 351 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25531393
[Au] Autor:Luo WW; Lian H; Zhong B; Shu HB; Li S
[Ti] Título:Krüppel-like factor 4 negatively regulates cellular antiviral immune response.
[So] Source:Cell Mol Immunol;13(1):65-72, 2016 Jan.
[Is] ISSN:2042-0226
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Viral infection triggers activation of the transcription factors NF-κB and IRF3, which collaborate to induce the expression of type I interferons (IFNs) and elicit innate antiviral response. In this report, we identified Krüppel-like factor 4 (KLF4) as a negative regulator of virus-triggered signaling. Overexpression of KLF4 inhibited virus-induced activation of ISRE and IFN-ß promoter in various types of cells, while knockdown of KLF4 potentiated viral infection-triggered induction of IFNB1 and downstream genes and attenuated viral replication. In addition, KLF4 was found to be localized in the cytosol and nucleus, and viral infection promoted the translocation of KLF4 from cytosol to nucleus. Upon virus infection, KLF4 was bound to the promoter of IFNB gene and inhibited the recruitment of IRF3 to the IFNB promoter. Our study thus suggests that KLF4 negatively regulates cellular antiviral response.
[Mh] Termos MeSH primário: Vírus da Ectromelia/imunologia
Interações Hospedeiro-Patógeno
Interferon beta/imunologia
Fatores de Transcrição Kruppel-Like/imunologia
Vírus Sendai/imunologia
[Mh] Termos MeSH secundário: Fracionamento Celular
Núcleo Celular/imunologia
Núcleo Celular/virologia
Imunoprecipitação da Cromatina
Citosol/imunologia
Citosol/virologia
Vírus da Ectromelia/crescimento & desenvolvimento
Regulação da Expressão Gênica
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Células HEK293
Seres Humanos
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Interferon beta/genética
Fatores de Transcrição Kruppel-Like/antagonistas & inibidores
Fatores de Transcrição Kruppel-Like/genética
Luciferases/genética
Luciferases/metabolismo
NF-kappa B/genética
NF-kappa B/imunologia
Regiões Promotoras Genéticas
Transporte Proteico
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Vírus Sendai/crescimento & desenvolvimento
Transdução de Sinais
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GKLF protein); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Kruppel-Like Transcription Factors); 0 (NF-kappa B); 0 (RNA, Small Interfering); 147336-22-9 (Green Fluorescent Proteins); 77238-31-4 (Interferon-beta); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160115
[Lr] Data última revisão:
160115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141223
[St] Status:MEDLINE
[do] DOI:10.1038/cmi.2014.125



página 1 de 36 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde