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Pesquisa : D12.644.276.374.440.890.275 [Categoria DeCS]
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[PMID]:28461106
[Au] Autor:Staun-Ram E; Miller A
[Ad] Endereço:Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
[Ti] Título:Effector and regulatory B cells in Multiple Sclerosis.
[So] Source:Clin Immunol;184:11-25, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of B cells in the pathogenesis of Multiple Sclerosis (MS), an autoimmune neurodegenerative disease, is becoming eminent in recent years, but the specific contribution of the distinct B cell subsets remains to be elucidated. Several B cell subsets have shown regulatory, anti-inflammatory capacities in response to stimuli in vitro, as well as in the animal model of MS: Experimental Autoimmune Encephalomyelitis (EAE). However, the functional role of the B regulatory cells (Bregs) in vivo and specifically in the human disease is yet to be clarified. In the present review, we have summarized the updated information on the roles of effector and regulatory B cells in MS and the immune-modulatory effects of MS therapeutic agents on their phenotype and function.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos B/imunologia
Linfócitos B Reguladores/imunologia
Encefalomielite Autoimune Experimental/imunologia
Esclerose Múltipla/imunologia
[Mh] Termos MeSH secundário: Alemtuzumab/uso terapêutico
Animais
Crotonatos/uso terapêutico
Fumarato de Dimetilo/uso terapêutico
Cloridrato de Fingolimode/uso terapêutico
Acetato de Glatiramer/uso terapêutico
Seres Humanos
Fatores Imunológicos/uso terapêutico
Imunossupressores/uso terapêutico
Interferon beta/uso terapêutico
Esclerose Múltipla/tratamento farmacológico
Natalizumab/uso terapêutico
Rituximab/uso terapêutico
Toluidinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Crotonates); 0 (Immunologic Factors); 0 (Immunosuppressive Agents); 0 (Natalizumab); 0 (Toluidines); 1C058IKG3B (teriflunomide); 3A189DH42V (Alemtuzumab); 4F4X42SYQ6 (Rituximab); 5M691HL4BO (Glatiramer Acetate); 77238-31-4 (Interferon-beta); FO2303MNI2 (Dimethyl Fumarate); G926EC510T (Fingolimod Hydrochloride)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28464285
[Au] Autor:Huang H; Zhang N; Xiong Q; Chen R; Zhang C; Wang N; Wang L; Ren H; Liu M; Qian M; Du B
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
[Ti] Título:Elimination of GPR146-mediated antiviral function through IRF3/HES1-signalling pathway.
[So] Source:Immunology;152(1):102-114, 2017 09.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:As the most important host defence against viral infection, interferon (IFN) stimulates hundreds of antiviral genes (ISGs) that together establish an 'antiviral state'. However, the antiviral function of most ISGs in viral infection still need further exploration. Here, we demonstrated that the expression of G-protein-coupled receptor 146 (GPR146) is highly increased by both IFN-ß and IFN-γ in a signal transducer and activator of transcription 1-dependent signalling pathway. Most importantly, overexpression of GPR146 protects the host cells from vesicular stomatitis virus and Newcastle disease virus infection but not from infection by herpes simplex virus. In contrast, the virus-induced IFN-ß production changed little in Gpr146-knockout cells. Furthermore, the Gpr146-deficient mice showed similar susceptibility to wild-type mice with vesicular stomatitis virus infection. Interestingly, the expression of GPR146 in virus-infected cells was strikingly reduced and can partially explain why the viral infection was little influenced in Gpr146-knockout mice. Surprisingly, virus-activated IFN regulatory factor 3 (IRF3) signalling not only induces the expression of IFN but also represses GPR146 expression through HES1 (hairy and enhancer of split-1)-mediated transcriptional activity to establish a dynamic equilibrium between pro-viral and antiviral stages in host cells. Taken together, these data reveal the antiviral role of GPR146 in fighting viral infection although the GPR146-mediated protection is eliminated by IRF3/HES1-signalling, which suggests a potential therapeutic significance of both GPR146 and HES1 signalling in viral infection.
[Mh] Termos MeSH primário: Herpes Simples/prevenção & controle
Fator Regulador 3 de Interferon/metabolismo
Macrófagos Peritoneais/metabolismo
Doença de Newcastle/prevenção & controle
Receptores Acoplados a Proteínas-G/deficiência
Transdução de Sinais
Fatores de Transcrição HES-1/metabolismo
Estomatite Vesicular/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Cercopithecus aethiops
Genótipo
Células HEK293
Herpes Simples/imunologia
Herpes Simples/metabolismo
Herpes Simples/virologia
Herpesvirus Humano 1/imunologia
Herpesvirus Humano 1/metabolismo
Interações Hospedeiro-Patógeno
Seres Humanos
Fator Regulador 3 de Interferon/imunologia
Interferon beta/farmacologia
Interferon gama/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Macrófagos Peritoneais/imunologia
Macrófagos Peritoneais/virologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Doença de Newcastle/imunologia
Doença de Newcastle/metabolismo
Doença de Newcastle/virologia
Vírus da Doença de Newcastle/imunologia
Vírus da Doença de Newcastle/metabolismo
Fenótipo
Células RAW 264.7
Interferência de RNA
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/imunologia
Fatores de Transcrição HES-1/imunologia
Transfecção
Células Vero
Estomatite Vesicular/imunologia
Estomatite Vesicular/metabolismo
Estomatite Vesicular/virologia
Vírus da Estomatite Vesicular Indiana/imunologia
Vírus da Estomatite Vesicular Indiana/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (G protein-coupled receptor 146, mouse); 0 (Hes1 protein, mouse); 0 (IFNG protein, mouse); 0 (Interferon Regulatory Factor-3); 0 (Irf3 protein, mouse); 0 (Receptors, G-Protein-Coupled); 0 (Transcription Factor HES-1); 77238-31-4 (Interferon-beta); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12752


  3 / 8371 MEDLINE  
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[PMID]:28461567
[Au] Autor:Saleh D; Najjar M; Zelic M; Shah S; Nogusa S; Polykratis A; Paczosa MK; Gough PJ; Bertin J; Whalen M; Fitzgerald KA; Slavov N; Pasparakis M; Balachandran S; Kelliher M; Mecsas J; Degterev A
[Ad] Endereço:Medical Scientist Training Program, Sackler School of Graduate Biomedical Sciences, Tufts University School of Medicine, Boston, MA 02111.
[Ti] Título:Kinase Activities of RIPK1 and RIPK3 Can Direct IFN-ß Synthesis Induced by Lipopolysaccharide.
[So] Source:J Immunol;198(11):4435-4447, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The innate immune response is a central element of the initial defense against bacterial and viral pathogens. Macrophages are key innate immune cells that upon encountering pathogen-associated molecular patterns respond by producing cytokines, including IFN-ß. In this study, we identify a novel role for RIPK1 and RIPK3, a pair of homologous serine/threonine kinases previously implicated in the regulation of necroptosis and pathologic tissue injury, in directing IFN-ß production in macrophages. Using genetic and pharmacologic tools, we show that catalytic activity of RIPK1 directs IFN-ß synthesis induced by LPS in mice. Additionally, we report that RIPK1 kinase-dependent IFN-ß production may be elicited in an analogous fashion using LPS in bone marrow-derived macrophages upon inhibition of caspases. Notably, this regulation requires kinase activities of both RIPK1 and RIPK3, but not the necroptosis effector protein, MLKL. Mechanistically, we provide evidence that necrosome-like RIPK1 and RIPK3 aggregates facilitate canonical TRIF-dependent IFN-ß production downstream of the LPS receptor TLR4. Intriguingly, we also show that RIPK1 and RIPK3 kinase-dependent synthesis of IFN-ß is markedly induced by avirulent strains of Gram-negative bacteria, and , and less so by their wild-type counterparts. Overall, these observations identify unexpected roles for RIPK1 and RIPK3 kinases in the production of IFN-ß during the host inflammatory responses to bacterial infection and suggest that the axis in which these kinases operate may represent a target for bacterial virulence factors.
[Mh] Termos MeSH primário: Interferon beta/biossíntese
Lipopolissacarídeos/imunologia
Macrófagos/imunologia
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/imunologia
Bactérias Gram-Negativas/imunologia
Interferon beta/imunologia
Klebsiella/imunologia
Macrófagos/microbiologia
Camundongos
Necrose/imunologia
Fosforilação
Receptor 4 Toll-Like/imunologia
Yersinia/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 77238-31-4 (Interferon-beta); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 2.7.11.1 (Ripk1 protein, mouse); EC 2.7.11.1 (Ripk3 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601717


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[PMID]:29320652
[Au] Autor:Reich DS; Lucchinetti CF; Calabresi PA
[Ad] Endereço:From the Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda (D.S.R.), and the Departments of Neurology and Neuroscience, Johns Hopkins School of Medicine, Baltimore (P.A.C.) - both in Maryland; and the Department of Neurology, Mayo Clinic, Rochester, MN (C.F.L.).
[Ti] Título:Multiple Sclerosis.
[So] Source:N Engl J Med;378(2):169-180, 2018 01 11.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Encéfalo/patologia
Fatores Imunológicos/uso terapêutico
Esclerose Múltipla
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/uso terapêutico
Biomarcadores
Acetato de Glatiramer/uso terapêutico
Seres Humanos
Interferon beta/uso terapêutico
Imagem por Ressonância Magnética
Esclerose Múltipla/diagnóstico por imagem
Esclerose Múltipla/tratamento farmacológico
Esclerose Múltipla/etiologia
Esclerose Múltipla/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Biomarkers); 0 (Immunologic Factors); 5M691HL4BO (Glatiramer Acetate); 77238-31-4 (Interferon-beta)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMra1401483


  5 / 8371 MEDLINE  
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[PMID]:28471483
[Au] Autor:Gao L; Bird AK; Meednu N; Dauenhauer K; Liesveld J; Anolik J; Looney RJ
[Ad] Endereço:University of Rochester Medical Center, Rochester, New York.
[Ti] Título:Bone Marrow-Derived Mesenchymal Stem Cells From Patients With Systemic Lupus Erythematosus Have a Senescence-Associated Secretory Phenotype Mediated by a Mitochondrial Antiviral Signaling Protein-Interferon-ß Feedback Loop.
[So] Source:Arthritis Rheumatol;69(8):1623-1635, 2017 08.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Bone marrow-derived mesenchymal stem cells (BM-MSCs) create a special microenvironment for hematopoiesis and immunity and display robust immunomodulatory properties that are impaired in systemic lupus erythematosus (SLE). This study was undertaken to identify the mechanisms of defects in human SLE BM-MSCs. METHODS: Patients fulfilling SLE classification criteria and healthy controls (n = 6 per group) were recruited according to an institutional review board-approved protocol. BM-MSCs were isolated with low-density Ficoll-Hypaque, verified by flow cytometry, and studied using immunocytochemistry, real-time polymerase chain reaction, Western blotting, comet assay, ß-galactosidase assay, and RNA interference. RESULTS: SLE BM-MSCs had a senescent phenotype characterized by a reduced proliferation rate, increased production of reactive oxygen species, increased DNA damage and repair, increased expression of p53 and p16, which block the cell cycle, and altered cytokine production (increased proinflammatory cytokine production and decreased immunomodulatory cytokine production). Moreover, SLE BM-MSCs had a 5-fold increase in interferon-ß (IFNß) levels (P < 0.05 versus healthy controls) and increased IFNß-induced messenger RNAs (mRNAs), including mRNA for the intracellular nucleic acid-sensing adaptor protein mitochondrial antiviral signaling protein (MAVS), whose expression was highly correlated with IFNß levels (r > 0.9, P < 0.01). Since MAVS is known to induce IFNß production, we hypothesized that there is a positive feedback loop between MAVS and IFNß. Notably, silencing of MAVS markedly decreased IFNß, p53, and p16 protein levels and expression of mRNAs for proinflammatory cytokines. CONCLUSION: This study demonstrates a novel pathway for elevated IFNß signaling in SLE that is not dependent on stimulation by immune complexes but rather is cell intrinsic and critically mediated by IFNß and MAVS, implicating new pathways as potential therapeutic targets.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/imunologia
Senescência Celular/imunologia
Interferon beta/imunologia
Lúpus Eritematoso Sistêmico/imunologia
Células Mesenquimais Estromais/imunologia
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Adulto
Western Blotting
Medula Óssea
Senescência Celular/genética
Inibidor p16 de Quinase Dependente de Ciclina/metabolismo
Citocinas/genética
Citocinas/imunologia
Retroalimentação
Feminino
Citometria de Fluxo
Seres Humanos
Interferon beta/genética
Lúpus Eritematoso Sistêmico/genética
Lúpus Eritematoso Sistêmico/metabolismo
Células Mesenquimais Estromais/metabolismo
Meia-Idade
Fenótipo
Interferência de RNA
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (Cytokines); 0 (P16 protein, human); 0 (RNA, Messenger); 0 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 0 (VISA protein, human); 77238-31-4 (Interferon-beta)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/art.40142


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[PMID]:28455446
[Au] Autor:Wang C; Sun M; Yuan X; Ji L; Jin Y; Cardona CJ; Xing Z
[Ad] Endereço:From the Medical School and Jiangsu Provincial Key Laboratory of Medicine, Nanjing University, Nanjing 210008, China.
[Ti] Título:Enterovirus 71 suppresses interferon responses by blocking Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling through inducing karyopherin-α1 degradation.
[So] Source:J Biol Chem;292(24):10262-10274, 2017 06 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enterovirus 71 (EV71) has emerged as one of the most important enteroviruses since the eradication of poliovirus, and it causes severe neurological symptoms for which no effective antiviral drugs are available. Type I interferons (IFN) α/ß have been used clinically as antiviral therapy as the first line of defense against virus infections successfully for decades. However, treatment with type I interferons has not been effective in patients with EV71 infection. In this study, we found that in cells pretreated with IFN-ß, EV71 infection could still lead to a cytopathic effect, and the viral replication was not affected. The mechanism by which EV71 antagonizes interferon signaling, however, has been controversial. Our study indicated that EV71 infection did not inhibit phosphorylation of STAT1/2 induced by IFN-ß stimulation, but p-STAT1/2 transport into the nucleus was significantly blocked. We showed that EV71 infection reduced the formation of STAT/karyopherin-α1 (KPNA1) complex upon interferon stimulation and that the virus down-regulated the expression of KPNA1, a nuclear localization signal receptor for p-STAT1. Using specific caspase inhibitors and siRNA for caspase-3, we demonstrated that EV71 infection induced degradation of cellular KPNA1 in a caspase-3-dependent manner, which led to decreased induction of interferon-inducible genes and IFN response. Viral 2A and 3C proteases did not degrade KPNA1, inhibit the activity of ISRE or suppress the transcription of interferon-inducible genes induced by IFN-ß. Our study demonstrates a novel mechanism by which antiviral signaling is suppressed through degradation of KPNA1 by activated caspase-3 induced in an enteroviral infection.
[Mh] Termos MeSH primário: Caspase 3/metabolismo
Enterócitos/virologia
Enterovirus Humano A/fisiologia
Interferon beta/metabolismo
Janus Quinase 1/metabolismo
Transdução de Sinais
alfa Carioferinas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular
Animais
Caspase 3/química
Caspase 3/genética
Cercopithecus aethiops
Enterócitos/imunologia
Enterócitos/metabolismo
Enterovirus Humano A/crescimento & desenvolvimento
Células HT29
Células HeLa
Seres Humanos
Interferon beta/genética
Janus Quinase 1/genética
Fosforilação
Processamento de Proteína Pós-Traducional
Proteólise
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT2/metabolismo
Células Vero
Replicação Viral
alfa Carioferinas/genética
alfa Carioferinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KPNA1 protein, human); 0 (Recombinant Fusion Proteins); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT2 Transcription Factor); 0 (STAT2 protein, human); 0 (alpha Karyopherins); 77238-31-4 (Interferon-beta); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (Janus Kinase 1); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171228
[Lr] Data última revisão:
171228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.745729


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[PMID]:27777077
[Au] Autor:Chen Y; Jiao B; Yao M; Shi X; Zheng Z; Li S; Chen L
[Ad] Endereço:Institute of Blood Transfusion, Chinese Academy of Medical Sciences and Peking Union Medical College, Provincial Key Laboratory for Transfusion-transmitted Infectious Diseases of Sichuan Province, Chengdu, Sichuan, 610052 China.
[Ti] Título:ISG12a inhibits HCV replication and potentiates the anti-HCV activity of IFN-α through activation of the Jak/STAT signaling pathway independent of autophagy and apoptosis.
[So] Source:Virus Res;227:231-239, 2017 01 02.
[Is] ISSN:1872-7492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Interferon stimulated (sensitive) genes (ISGs) are the effector molecules downstream of type I/III interferon (IFN) signaling pathways in host innate immunity. ISG12a can be induced by IFN-α. Although ISG12a has been reported to inhibit the replication of HCV, the exact mechanism remains to be determined. In this study, we investigated the possible mechanisms of ISG12a anti- HCV property by exploring the production of type I IFN and the activation of Janus kinase/signal transducer and activator of transcription (Jak/STAT) signaling pathway, apoptosis and autophagy in Huh7.5.1 cells transiently transfected with ISG12a over-expression plasmid. Interestingly, we found that ISG12a inhibited HCV replication in both Con1b replicon and the HCV JFH1-based cell culture system and potentiated the anti-HCV activity of IFN-α. ISG12a promoted the production of IFN α/ß and activated the type I IFN signaling pathway as shown by increased p-STAT1 level, higher Interferon sensitive response element (ISRE) activity and up-regulated ISG levels. However, ISG12a over-expression did not affect cell autophagy and apoptosis. Data from our current study collectively indicated that ISG12a inhibited HCV replication and potentiated the anti-HCV activity of IFN-α possibly through induced production of type I IFNs and activation of Jak/STAT signaling pathway independent of autophagy and cell apoptosis.
[Mh] Termos MeSH primário: Hepacivirus/fisiologia
Interferon-alfa/metabolismo
Janus Quinases/metabolismo
Proteínas de Membrana/metabolismo
Fatores de Transcrição STAT/metabolismo
Transdução de Sinais
Replicação Viral
[Mh] Termos MeSH secundário: Apoptose/genética
Autofagia/genética
Linhagem Celular
Células Cultivadas
Expressão Gênica
Hepatite C/genética
Hepatite C/metabolismo
Hepatite C/virologia
Seres Humanos
Interferon Tipo I/biossíntese
Interferon beta/metabolismo
Proteínas de Membrana/genética
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IFI27 protein, human); 0 (Interferon Type I); 0 (Interferon-alpha); 0 (Membrane Proteins); 0 (STAT Transcription Factors); 77238-31-4 (Interferon-beta); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  8 / 8371 MEDLINE  
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[PMID]:29040311
[Au] Autor:Kondoh T; Manzoor R; Nao N; Maruyama J; Furuyama W; Miyamoto H; Shigeno A; Kuroda M; Matsuno K; Fujikura D; Kajihara M; Yoshida R; Igarashi M; Takada A
[Ad] Endereço:Division of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
[Ti] Título:Putative endogenous filovirus VP35-like protein potentially functions as an IFN antagonist but not a polymerase cofactor.
[So] Source:PLoS One;12(10):e0186450, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It has been proposed that some non-retroviral RNA virus genes are integrated into vertebrate genomes. Endogenous filovirus-like elements (EFLs) have been discovered in some mammalian genomes. However, their potential roles in ebolavirus infection are unclear. A filovirus VP35-like element (mlEFL35) is found in the little brown bat (Myotis lucifugus) genome. Putative mlEFL35-derived protein (mlEFL35p) contains nearly full-length amino acid sequences corresponding to ebolavirus VP35. Ebola virus VP35 has been shown to bind double-stranded RNA, leading to inhibition of type I interferon (IFN) production, and is also known as a viral polymerase cofactor that is essential for viral RNA transcription/replication. In this study, we transiently expressed mlEFL35p in human kidney cells and investigated its biological functions. We first found that mlEFL35p was coimmunoprecipitated with itself and ebolavirus VP35s but not with the viral nucleoprotein. Then the biological functions of mlEFL35p were analyzed by comparing it to ebolavirus VP35s. We found that the expression of mlEFL35p significantly inhibited human IFN-ß promoter activity as well as VP35s. By contrast, expression of mlEFL35p did not support viral RNA transcription/replication and indeed slightly decrease the reporter gene expression in a minigenome assay. These results suggest that mlEFL35p potentially acts as an IFN antagonist but not a polymerase cofactor.
[Mh] Termos MeSH primário: Ebolavirus/genética
Interações Hospedeiro-Patógeno
Interferon beta/antagonistas & inibidores
Nucleoproteínas/genética
RNA de Cadeia Dupla/genética
Proteínas do Core Viral/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Quirópteros/virologia
Ebolavirus/isolamento & purificação
Ebolavirus/metabolismo
Expressão Gênica
Genes Reporter
Células HEK293
Seres Humanos
Interferon beta/genética
Interferon beta/imunologia
Luciferases/genética
Luciferases/metabolismo
Nucleoproteínas/metabolismo
Regiões Promotoras Genéticas
Ligação Proteica
RNA de Cadeia Dupla/metabolismo
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Proteínas do Core Viral/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nucleoproteins); 0 (RNA, Double-Stranded); 0 (Recombinant Proteins); 0 (Viral Core Proteins); 0 (nucleoprotein VP35, Ebola virus); 77238-31-4 (Interferon-beta); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186450


  9 / 8371 MEDLINE  
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[PMID]:29017920
[Au] Autor:Cho J; Yi H; Jang EY; Lee MS; Lee JY; Kang C; Lee CH; Kim K
[Ad] Endereço:Division of Viral Disease Research, Center for Infectious Diseases Research, Korea National Institute of Health, Cheongju, Republic of Korea; Department of Microbiology, Chungbuk National University, Cheongju, Republic of Korea.
[Ti] Título:Mycophenolic mofetil, an alternative antiviral and immunomodulator for the highly pathogenic avian influenza H5N1 virus infection.
[So] Source:Biochem Biophys Res Commun;494(1-2):298-304, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection with the highly pathogenic avian influenza H5N1 virus results in a high incidence of mortality in humans. Severe complications from infection are often associated with hypercytokinemia. However, current neuraminidase inhibitors (NAIs) have several limitations including the appearance of oseltamivir-resistant H5N1 virus and the inability to completely ameliorate hyper-immune responses. To overcome these limitations, we evaluated the anti-viral activity of mycophenolic mofetil (MMF) against A/Vietnam/1194/2004 (H5N1) virus infection using MDCK cells and mice. The IC of MMF (0.94 µM) was comparable to that of zanamivir (0.87 µM) in H5N1 virus-infected MDCK cells based on ELISA. Time-course assays demonstrated that MMF completely inhibited H5N1 viral mRNA replication and protein expression for approximately 8 h after the initiation of treatment. In addition, MMF treatment protected 100% of mice, and lung viral titers were substantially reduced. The anti-viral mechanism of MMF against H5N1 virus infection was further confirmed to depend on the inhibition of cellular inosine monophosphate dehydrogenase (IMPDH) by exogenous guanosine, which inhibits viral mRNA and protein expression. Moreover, IL-1ß, IFN-ß, IL-6, and IP-10 mRNA expression levels were significantly downregulated in MDCK cells with MMF treatment. These results indicated that MMF could represent a novel inhibitor of viral replication and a potent immunomodulator for the treatment of H5N1 virus infection.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Fatores Imunológicos/farmacologia
Vírus da Influenza A Subtipo H5N1/efeitos dos fármacos
Ácido Micofenólico/farmacologia
Infecções por Orthomyxoviridae/tratamento farmacológico
Oseltamivir/farmacologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL10/antagonistas & inibidores
Quimiocina CXCL10/genética
Quimiocina CXCL10/imunologia
Embrião de Galinha
Cães
Feminino
Regulação da Expressão Gênica
Interações Hospedeiro-Patógeno/efeitos dos fármacos
IMP Desidrogenase/antagonistas & inibidores
IMP Desidrogenase/genética
IMP Desidrogenase/imunologia
Vírus da Influenza A Subtipo H5N1/crescimento & desenvolvimento
Vírus da Influenza A Subtipo H5N1/patogenicidade
Interferon beta/antagonistas & inibidores
Interferon beta/genética
Interferon beta/imunologia
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/genética
Interleucina-1beta/imunologia
Interleucina-6/antagonistas & inibidores
Interleucina-6/genética
Interleucina-6/imunologia
Pulmão/efeitos dos fármacos
Pulmão/imunologia
Pulmão/virologia
Células Madin Darby de Rim Canino
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Orthomyxoviridae/imunologia
Infecções por Orthomyxoviridae/mortalidade
Infecções por Orthomyxoviridae/patologia
RNA Viral/antagonistas & inibidores
RNA Viral/biossíntese
Análise de Sobrevida
Replicação Viral/efeitos dos fármacos
Zanamivir/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Chemokine CXCL10); 0 (Cxcl10 protein, mouse); 0 (IL1B protein, mouse); 0 (Immunologic Factors); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (RNA, Viral); 0 (interleukin-6, mouse); 20O93L6F9H (Oseltamivir); 77238-31-4 (Interferon-beta); EC 1.1.1.205 (IMP Dehydrogenase); HU9DX48N0T (Mycophenolic Acid); L6O3XI777I (Zanamivir)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE


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[PMID]:28954259
[Au] Autor:Cui H; Liu Y; Huang Y
[Ad] Endereço:Department of Ophthalmology, Chinese PLA General Hospital, Beijing, China.
[Ti] Título:Roles of TRIM32 in Corneal Epithelial Cells After Infection with Herpes Simplex Virus.
[So] Source:Cell Physiol Biochem;43(2):801-811, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Epithelial cells play important roles as a critical barrier in protecting the cornea from microbial pathogens infection. METHODS: In this study, we were aiming to investigate the role of E3 ubiquitin ligase tripartite motif protein 32 (TRIM32) in corneal epithelial cells in response to Herpes Simplex Virus type 1 (HSV-1) infection and to elucidate the underlying mechanisms. RESULTS: We found the expression of TRIM32 was increased after infected with HSV-1 both in murine corneas and cultured human epithelial (HCE) cells. Furthermore, knockdown of the expression of TRIM32 significantly aggravated HSV-1 induced herpetic stromal keratitis (HSK) in mice and promoted the replication of HSV-1 in cultured HCE cells. We also observed that silencing of TRIM32 resulted in the decreased expression of IFN-ß and suppressed activation of interferon regulatory factor 3 (IRF3) both in vivo and in vitro. Finally, we found TRIM32 positively regulate IFN-ß production in corneal epithelial cells through promoting K63-linked polyubiquitination of stimulator of interferon genes (STING). CONCLUSION: In conclusion, our data suggested that TRIM32 as a crucial positive regulator of HSV-1 induced IFN-ß production in corneal epithelial cells, and it played a predominant role in clearing HSV-1 from the cornea.
[Mh] Termos MeSH primário: Córnea/virologia
Herpesvirus Humano 1/fisiologia
Ceratite Herpética/metabolismo
Fatores de Transcrição/metabolismo
Proteínas com Motivo Tripartido/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Córnea/metabolismo
Córnea/patologia
Regulação para Baixo
Feminino
Seres Humanos
Fator Regulador 3 de Interferon/metabolismo
Interferon beta/genética
Interferon beta/metabolismo
Ceratite Herpética/genética
Ceratite Herpética/patologia
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Poliubiquitina/metabolismo
Fatores de Transcrição/genética
Proteínas com Motivo Tripartido/genética
Ubiquitina-Proteína Ligases/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Regulatory Factor-3); 0 (MPYS protein, mouse); 0 (Membrane Proteins); 0 (Transcription Factors); 0 (Tripartite Motif Proteins); 120904-94-1 (Polyubiquitin); 77238-31-4 (Interferon-beta); EC 2.3.2.27 (TRIM32 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 6.3.2.19 (TRIM32 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1159/000481563



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