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[PMID]:26136579
[Au] Autor:Butchi N; Kapil P; Puntambekar S; Stohlman SA; Hinton DR; Bergmann CC
[Ad] Endereço:Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
[Ti] Título:Myd88 Initiates Early Innate Immune Responses and Promotes CD4 T Cells during Coronavirus Encephalomyelitis.
[So] Source:J Virol;89(18):9299-312, 2015 Sep.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Myd88 signaling is critical to the control of numerous central nervous system (CNS) infections by promoting both innate and adaptive immune responses. Nevertheless, the extent to which Myd88 regulates type I interferon (IFN) versus proinflammatory factors and T cell function, as well as the anatomical site of action, varies extensively with the pathogen. CNS infection by neurotropic coronavirus with replication confined to the brain and spinal cord induces protective IFN-α/ß via Myd88-independent activation of melanoma differentiation-associated gene 5 (MDA5). However, a contribution of Myd88-dependent signals to CNS pathogenesis has not been assessed. Infected Myd88(-/-) mice failed to control virus, exhibited enhanced clinical disease coincident with increased demyelination, and succumbed to infection within 3 weeks. The induction of IFN-α/ß, as well as of proinflammatory cytokines and chemokines, was impaired early during infection. However, defects in both IFN-α/ß and select proinflammatory factors were rapidly overcome prior to T cell recruitment. Myd88 deficiency also specifically blunted myeloid and CD4 T cell recruitment into the CNS without affecting CD8 T cells. Moreover, CD4 T cells but not CD8 T cells were impaired in IFN-γ production. Ineffective virus control indeed correlated most prominently with reduced antiviral IFN-γ in the CNS of Myd88(-/-) mice. The results demonstrate a crucial role for Myd88 both in early induction of innate immune responses during coronavirus-induced encephalomyelitis and in specifically promoting protective CD4 T cell activation. In the absence of these responses, functional CD8 T cells are insufficient to control viral spread within the CNS, resulting in severe demyelination. IMPORTANCE: During central nervous system (CNS) infections, signaling through the adaptor protein Myd88 promotes both innate and adaptive immune responses. The extent to which Myd88 regulates antiviral type I IFN, proinflammatory factors, adaptive immunity, and pathology is pathogen dependent. These results reveal that Myd88 protects from lethal neurotropic coronavirus-induced encephalomyelitis by accelerating but not enhancing the induction of IFN-α/ß, as well as by promoting peripheral activation and CNS accumulation of virus-specific CD4 T cells secreting IFN-γ. By controlling both early innate immune responses and CD4 T cell-mediated antiviral IFN-γ, Myd88 signaling limits the initial viral dissemination and is vital for T cell-mediated control of viral loads. Uncontrolled viral replication in the absence of Myd88 leads to severe demyelination and pathology despite overall reduced inflammatory responses. These data support a vital role of Myd88 signaling in protective antimicrobial functions in the CNS by promoting proinflammatory mediators and T cell-mediated IFN-γ production.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Infecções por Coronavirus/imunologia
Encefalite Viral/imunologia
Imunidade Celular
Imunidade Inata
Vírus Elberfeld do Camundongo/imunologia
Fator 88 de Diferenciação Mieloide/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/patologia
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Infecções por Coronavirus/genética
Infecções por Coronavirus/patologia
Encefalite Viral/genética
Encefalite Viral/patologia
Interferon-alfa/genética
Interferon-alfa/imunologia
Interferon beta/genética
Interferon beta/imunologia
Vírus Elberfeld do Camundongo/genética
Camundongos
Camundongos Knockout
Fator 88 de Diferenciação Mieloide/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Interferon-alpha); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 77238-31-4 (Interferon-beta)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150703
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01199-15


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[PMID]:24319751
[Au] Autor:Sokolova TM; Shuvalov AN; Telkov MV; Kolodyazhnaya LV; Ershov FI
[Ad] Endereço:N. F. Gamalea Institute of Epidemiology and Microbiology, Ministry of Health of the Russian Federation; D. I. Ivanoskii Institute of Virology, Ministry of Health of the Russian Federation, Moscow, Russia. tmsokolovavir@mail.ru.
[Ti] Título:Ridostin induces transcription of a wide spectrum of interferon genes in human cells.
[So] Source:Bull Exp Biol Med;156(2):213-6, 2013 Dec.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The effects of Ridostin on the transcription of IFN family genes in human fibroblasts and lymphocytes were studied by quantitative real-time PCR. The degree of gene induction by Ridostin was most pronounced in fibroblasts, and was significantly higher than the induction by Kagocel: transcription of IFN-ß, oligoadenylate synthetase, and double-stranded RNA-dependent protein kinase genes increased by about 2000, 100, and 20 times, respectively. In lymphocytes, Ridostin also activated a wide variety of IFN family genes, including genes of IFN-ß, IFN-γ, and IFN-dependent enzymes, but this induction was less pronounced than in the fibroblasts. It was shown that gene response in lymphocyte from a child with cancer is reduced in comparison with that of adult healthy participant. Ridostin, and even more so Reaferon up-regulated activities of ß-actin, glycerophosphate dehydrogenase, and ß2-microglobulin genes, thus making impossible or limiting their use as constitutive stable reference genes (standards) in PCR-assays of IFN and their inductors.
[Mh] Termos MeSH primário: Indutores de Interferon/farmacologia
Interferons/biossíntese
RNA de Cadeia Dupla/farmacologia
RNA Fúngico/farmacologia
Transcrição Genética/efeitos dos fármacos
Ativação Transcricional/efeitos dos fármacos
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/biossíntese
2',5'-Oligoadenilato Sintetase/genética
Actinas/biossíntese
Actinas/genética
Adulto
Antivirais/farmacologia
Linhagem Celular
Criança
Fibroblastos/metabolismo
Glicerolfosfato Desidrogenase/biossíntese
Glicerolfosfato Desidrogenase/genética
Gossipol/análogos & derivados
Gossipol/farmacologia
Seres Humanos
Interferon-alfa/farmacologia
Interferon beta/biossíntese
Interferon beta/genética
Interferon gama/biossíntese
Interferon gama/genética
Interferons/genética
Linfócitos/metabolismo
Vírus Elberfeld do Camundongo/efeitos dos fármacos
Proteínas Recombinantes/farmacologia
Microglobulina-2 beta/biossíntese
Microglobulina-2 beta/genética
eIF-2 Quinase/biossíntese
eIF-2 Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antiviral Agents); 0 (Interferon Inducers); 0 (Interferon-alpha); 0 (RNA, Double-Stranded); 0 (RNA, Fungal); 0 (Recombinant Proteins); 0 (beta 2-Microglobulin); 112279-02-4 (ridostin); 115774-57-7 (cagocel-1); 43K1W2T1M6 (interferon alfa-2b); 77238-31-4 (Interferon-beta); 82115-62-6 (Interferon-gamma); 9008-11-1 (Interferons); EC 1.1.- (Glycerolphosphate Dehydrogenase); EC 2.7.11.1 (eIF-2 Kinase); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase); KAV15B369O (Gossypol)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:161128
[Lr] Data última revisão:
161128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131210
[St] Status:MEDLINE


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[PMID]:24063184
[Au] Autor:Jiang L
[Ad] Endereço:Shanghai Qisheng Biological Preparation Co., Ltd, Shanghai, 201106, P.R. China. lixiajiang18@hotmail.com
[Ti] Título:[Technical study on inactivating/removing virus in collagen sponge].
[So] Source:Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi;27(7):885-8, 2013 Jul.
[Is] ISSN:1002-1892
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To verify the technics of inactivating/removing virus in collagen sponge derived from bovine Achilles tendon. METHODS: Possible pathogen species were determined according to the raw material of bovine Achilles tendon used in production, then vesicular stomatitis virus (VSV), theiler's mouse encephalomyelitis virus (TEMV), pseudorabies virus (PRV), and simian vacuolating virus 40 (SV40) were selected as indicator virus. Virus suspension was prepared in accordance with Technical Standard for Disinfection. 60Co radiation 25 kGy of collagen sponge was determined as inactivating/removing virus process according to the analysis of the manufacture process, the virus inactivation/removal effect was verified by the measurement of median tissue culture infective dose (TCID50) and showed by virus reduction factor (sample average values of numerical difference before and after processing). RESULTS: Reduction factors of VSV, TEMV, PRV, and SV40 after 60Co radiation 25 kGy were 5.646, 4.792, 5.042, and 5.292 logTCID50/0.1 mL (logs), respectively. Reduction factor of each indicator virus was greater than 4 logs, showing that 60Co irradiation 25 kGy can effectively inactivate and remove viruses. CONCLUSION: 60Co radiation 25 kGy of collagen sponge derived from bovine Achilles tendon can be used as the technics of inactivating/removing virus during the preparation process of collagen sponge to guarantee the safety of the product.
[Mh] Termos MeSH primário: Radioisótopos de Cobalto
Colágeno
Esterilização/métodos
Inativação de Vírus/efeitos da radiação
Vírus/efeitos da radiação
[Mh] Termos MeSH secundário: Tendão do Calcâneo/química
Tendão do Calcâneo/virologia
Animais
Bovinos
Linhagem Celular
Segurança de Produtos ao Consumidor
Equipamentos e Provisões Hospitalares
Esponja de Gelatina Absorvível
Herpesvirus Suídeo 1/efeitos da radiação
Vírus Elberfeld do Camundongo/efeitos da radiação
Vírus 40 dos Símios/efeitos da radiação
Vesiculovirus/efeitos da radiação
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cobalt Radioisotopes); 9007-34-5 (Collagen)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:130925
[Lr] Data última revisão:
130925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130926
[St] Status:MEDLINE


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[PMID]:23513048
[Au] Autor:Buskiewicz IA; Huber SA
[Ti] Título:MDA5: the almighty for Myocardium.
[So] Source:Circ Heart Fail;6(2):153-5, 2013 Mar.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Infecções por Cardiovirus/metabolismo
RNA Helicases DEAD-box/metabolismo
Vírus Elberfeld do Camundongo/patogenicidade
Miocardite/prevenção & controle
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Helicase IFIH1 Induzida por Interferon
Masculino
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
EC 3.6.1.- (Ifih1 protein, mouse); EC 3.6.4.13 (DEAD-box RNA Helicases); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130321
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCHEARTFAILURE.113.000137


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[PMID]:23271791
[Au] Autor:Philip J; Xu Z; Bowles NE; Vallejo JG
[Ad] Endereço:Department of Pediatrics, Sections of Infectious Diseases, and Critical Care Medicine, Baylor College of Medicine and Texas Children's Hospital, Houston, TX 77030, USA.
[Ti] Título:Cardiac-specific overexpression of melanoma differentiation-associated gene-5 protects mice from lethal viral myocarditis.
[So] Source:Circ Heart Fail;6(2):326-34, 2013 Mar.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Viral myocarditis is among the most common causes of heart failure in children and young adults. The RNA helicase melanoma differentiation-associated gene-5 (MDA5) is critical for host antiviral responses against members of the Picornaviridae family, such as encephalomyocarditis virus (EMCV). MDA5-knockout mice are highly susceptible to EMCV infection and develop significant myocardial injury and left ventricular dysfunction. However, the mechanisms by which MDA5 signaling within cardiac myocytes contributes to the host response against viral infection have not been defined. METHODS AND RESULTS: We generated cardiac-specific MDA5 transgenic (alpha-myosin heavy chain [αMHC]-MDA5) mice. These mice showed increased baseline cardiac expression of antiviral cytokines and increased cellular infiltration but no alterations in cardiac function and structure. αMHC-MDA5 mice were less susceptible to EMCV infection and had a significantly lower cardiac viral load compared with littermate control mice. The severity of myocarditis, prevalence of cardiac myocyte apoptosis, and cleavage of caspase 3 after EMCV infection were attenuated in αMHC-MDA5 mice. Furthermore, αMHC-MDA5 mice were protected against EMCV-induced myocardial dysfunction. CONCLUSIONS: Our data suggest that myocardial MDA5 may be a key molecule in protecting the heart from direct viral injury and myocardial dysfunction.
[Mh] Termos MeSH primário: Infecções por Cardiovirus/metabolismo
RNA Helicases DEAD-box/metabolismo
Vírus Elberfeld do Camundongo/patogenicidade
Miocardite/prevenção & controle
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Infecções por Cardiovirus/genética
Infecções por Cardiovirus/patologia
Infecções por Cardiovirus/fisiopatologia
Infecções por Cardiovirus/virologia
Caspase 3/metabolismo
RNA Helicases DEAD-box/deficiência
RNA Helicases DEAD-box/genética
Modelos Animais de Doenças
Feminino
Genótipo
Helicase IFIH1 Induzida por Interferon
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Miocardite/genética
Miocardite/metabolismo
Miocardite/patologia
Miocardite/fisiopatologia
Miocardite/virologia
Miocárdio/patologia
Fenótipo
Volume Sistólico
Fatores de Tempo
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/fisiopatologia
Disfunção Ventricular Esquerda/prevenção & controle
Disfunção Ventricular Esquerda/virologia
Função Ventricular Esquerda
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Caspase 3); EC 3.6.1.- (Ifih1 protein, mouse); EC 3.6.4.13 (DEAD-box RNA Helicases); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121229
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCHEARTFAILURE.112.969402


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[PMID]:20686046
[Au] Autor:Schmeisser H; Mejido J; Balinsky CA; Morrow AN; Clark CR; Zhao T; Zoon KC
[Ad] Endereço:Cytokine Biology Section, NIAID, MSC 8001, 50 Center Dr., Bldg. 50, Rm. 5515, Bethesda, MD 20892, USA.
[Ti] Título:Identification of alpha interferon-induced genes associated with antiviral activity in Daudi cells and characterization of IFIT3 as a novel antiviral gene.
[So] Source:J Virol;84(20):10671-80, 2010 Oct.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A novel assay was developed for Daudi cells in which the antiviral (AV) and antiproliferative (AP) activities of interferon (IFN) can be measured simultaneously. Using this novel assay, conditions allowing IFN AV protection but no growth inhibition were identified and selected. Daudi cells were treated under these conditions, and gene expression microarray analyses were performed. The results of the analysis identified 25 genes associated with IFN-α AV activity. Upregulation of 23 IFN-induced genes was confirmed by using reverse transcription-PCR. Of 25 gene products, 17 were detected by Western blotting at 24 h. Of the 25 genes, 10 have not been previously linked to AV activity of IFN-α. The most upregulated gene was IFIT3 (for IFN-induced protein with tetratricopeptide repeats 3). The results from antibody neutralizing experiments suggested an association of the identified genes with IFN-α AV activity. This association was strengthened by results from IFIT3-small interfering RNA transfection experiments showing decreased expression of IFIT3 and a reduction in the AV activity induced by IFN-α. Overexpression of IFIT3 resulted in a decrease of virus titer. Transcription of AV genes after the treatment of cells with higher concentrations of IFN having an AP effect on Daudi cells suggested pleiotropic functions of identified gene products.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Interferon Tipo I/farmacologia
Peptídeos e Proteínas de Sinalização Intracelular/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Linhagem Celular
Primers do DNA/genética
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/antagonistas & inibidores
Vírus Elberfeld do Camundongo/efeitos dos fármacos
Vírus Elberfeld do Camundongo/patogenicidade
Análise de Sequência com Séries de Oligonucleotídeos
Interferência de RNA
RNA Interferente Pequeno/genética
Proteínas Recombinantes
Regulação para Cima/efeitos dos fármacos
Vírus da Estomatite Vesicular Indiana/efeitos dos fármacos
Vírus da Estomatite Vesicular Indiana/patogenicidade
Viroses/tratamento farmacológico
Viroses/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (DNA Primers); 0 (IFIT3 protein, human); 0 (Interferon Type I); 0 (Intracellular Signaling Peptides and Proteins); 0 (RNA, Small Interfering); 0 (Recombinant Proteins)
[Em] Mês de entrada:1101
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100806
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.00818-10


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[PMID]:17600339
[Au] Autor:Hamo L; Stohlman SA; Otto-Duessel M; Bergmann CC
[Ad] Endereço:Department of Neuroscience, University of Southern California Keck School of Medicine, Los Angeles, California, USA.
[Ti] Título:Distinct regulation of MHC molecule expression on astrocytes and microglia during viral encephalomyelitis.
[So] Source:Glia;55(11):1169-77, 2007 Aug 15.
[Is] ISSN:0894-1491
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The potential interplay of glial cells with T cells during viral induced inflammation was assessed by comparing major histocompatibility complex molecule upregulation and retention on astrocytes and microglia. Transgenic mice expressing green fluorescent protein under control of the astrocyte-specific glial fibrillary acidic protein promoter were infected with a neurotropic coronavirus to facilitate phenotypic characterization of astrocytes and microglia using flow cytometry. Astrocytes in the adult central nervous system up-regulated class I surface expression, albeit delayed compared with microglia. Class II was barely detectable on astrocytes, in contrast to potent up-regulation on microglia. Maximal MHC expression in both glial cell types correlated with IFN-gamma levels and lymphocyte accumulation. Despite a decline of IFN-gamma concomitant to virus clearance, MHC molecule expression on glia was sustained. These data demonstrate distinct regulation of both class I and class II expression by microglia and astrocytes in vivo following viral induced inflammation. Furthermore, prolonged MHC expression subsequent to viral clearance implies a potential for ongoing presentation.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Encefalomielite/metabolismo
Regulação da Expressão Gênica/fisiologia
Genes MHC Classe II/genética
Genes MHC Classe I/genética
Microglia/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/patologia
Células Cultivadas
Encefalomielite/patologia
Encefalomielite/virologia
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Proteína Glial Fibrilar Ácida/genética
Proteínas de Fluorescência Verde/biossíntese
Proteínas de Fluorescência Verde/genética
Inflamação/patologia
Interferon gama/análise
Interferon gama/biossíntese
Masculino
Vírus Elberfeld do Camundongo
Camundongos
Camundongos Transgênicos
Microglia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 147336-22-9 (Green Fluorescent Proteins); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:0709
[Cu] Atualização por classe:081121
[Lr] Data última revisão:
081121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070630
[St] Status:MEDLINE


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[PMID]:17343922
[Au] Autor:Pachner AR; Li L; Narayan K
[Ad] Endereço:Department of Neurology and Neurosciences, UMDNJ-New Jersey Medical School, NJ, USA. pachner@umdnj.edu
[Ti] Título:Intrathecal antibody production in an animal model of multiple sclerosis.
[So] Source:J Neuroimmunol;185(1-2):57-63, 2007 Apr.
[Is] ISSN:0165-5728
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Although the central nervous system (CNS) is thought to be immunoprivileged, under special circumstances it can produce antibody. Antibody production within the CNS, called intrathecal antibody production (ITAbP), is a prominent feature of neurological infections and inflammatory diseases, and is thought to possibly contribute to disease in multiple sclerosis (MS), but it has not been extensively studied. We investigated ITAbP in a viral model of MS. ELISpot, real-time RT-PCR for IgG mRNA in CNS tissue, and CSF analysis were used to assess ITAbP in two types of SJL mice infected with one of two strains of Theiler's murine encephalomyelitis virus (TMEV). The amplitude of ITAbP increased during the first 4 months of infection. TMEV viral load remained high during the course of the infection, which likely was the main stimulus for ITAbP, since within samples of infected CNS tissues, levels of IgG gene expression were highly correlated with viral RNA levels, and a large percentage of intrathecally produced antibody was directed against TMEV. This study provides the first extensive analysis of ITAbP in TMEV infection, and demonstrates that, in this animal model of MS, antibody production within the CNS is likely driven by the presence of the causative pathogen.
[Mh] Termos MeSH primário: Anticorpos Antivirais/líquido cefalorraquidiano
Sistema Nervoso Central/imunologia
Imunoglobulina G/líquido cefalorraquidiano
Vírus Elberfeld do Camundongo/imunologia
Esclerose Múltipla/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antivirais/biossíntese
Formação de Anticorpos
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Feminino
Imunoglobulina G/biossíntese
Camundongos
RNA Mensageiro/análise
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Immunoglobulin G); 0 (RNA, Messenger)
[Em] Mês de entrada:0706
[Cu] Atualização por classe:070402
[Lr] Data última revisão:
070402
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070309
[St] Status:MEDLINE


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[PMID]:16809320
[Au] Autor:Ilyinskii PO; Wang R; Balk SP; Exley MA
[Ad] Endereço:Cancer Biology Program, Hematology/Oncology Division, Beth Israel Deaconess Medical Center, NRB 1030L, 330 Brookline Avenue, Boston, MA 02215, USA.
[Ti] Título:CD1d mediates T-cell-dependent resistance to secondary infection with encephalomyocarditis virus (EMCV) in vitro and immune response to EMCV infection in vivo.
[So] Source:J Virol;80(14):7146-58, 2006 Jul.
[Is] ISSN:0022-538X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The innate and adaptive immune responses have evolved distinct strategies for controlling different viral pathogens. Encephalomyocarditis virus (EMCV) is a picornavirus that can cause paralysis, diabetes, and myocarditis within days of infection. The optimal innate immune response against EMCV in vivo requires CD1d. Interaction of antigen-presenting cell CD1d with distinct natural killer T-cell ("NKT") populations can induce rapid gamma interferon (IFN-gamma) production and NK-cell activation. The T-cell response of CD1d-deficient mice (lacking all NKT cells) against acute EMCV infection was further studied in vitro and in vivo. EMCV persisted at higher levels in CD1d-knockout (KO) splenocyte cultures infected in vitro. Furthermore, optimal resistance to repeat cycles of EMCV infection in vitro was also shown to depend on CD1d. However, this was not reflected in the relative levels of NK-cell activation but rather by the responses of both CD4(+) and CD8(+) T-cell populations. Repeated EMCV infection in vitro induced less IFN-gamma and alpha interferon (IFN-alpha) from CD1d-deficient splenocytes than with the wild type. Furthermore, the level of EMCV replication in wild-type splenocytes was markedly and specifically increased by addition of blocking anti-CD1d antibody. Depletion experiments demonstrated that dendritic cells contributed less than the combination of NK and NKT cells to anti-EMCV responses and that none of these cell types was the main source of IFN-alpha. Finally, EMCV infection in vivo produced higher levels of viremia in CD1d-KO mice than in wild-type animals, coupled with significantly less lymphocyte activation and IFN-alpha production. These results point to the existence of a previously unrecognized mechanism of rapid CD1d-dependent stimulation of the antiviral adaptive cellular immune response.
[Mh] Termos MeSH primário: Antígenos CD1/imunologia
Linfócitos T CD4-Positivos/imunologia
Infecções por Cardiovirus/imunologia
Células Matadoras Naturais/imunologia
Ativação Linfocitária/imunologia
Vírus Elberfeld do Camundongo/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Anticorpos Monoclonais/imunologia
Anticorpos Monoclonais/farmacologia
Apresentação do Antígeno/imunologia
Antígenos CD1/genética
Antígenos CD1d
Linfócitos T CD4-Positivos/virologia
Infecções por Cardiovirus/genética
Diabetes Mellitus/imunologia
Diabetes Mellitus/virologia
Imunidade Inata/genética
Imunidade Inata/imunologia
Interferon-alfa/imunologia
Interferon gama/imunologia
Células Matadoras Naturais/virologia
Ativação Linfocitária/efeitos dos fármacos
Ativação Linfocitária/genética
Vírus Elberfeld do Camundongo/genética
Camundongos
Camundongos Knockout
Miocardite/imunologia
Miocardite/virologia
Paralisia/imunologia
Paralisia/virologia
Viremia/genética
Viremia/imunologia
Replicação Viral/efeitos dos fármacos
Replicação Viral/genética
Replicação Viral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD1); 0 (Antigens, CD1d); 0 (Interferon-alpha); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:0608
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060701
[St] Status:MEDLINE


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[PMID]:11769542
[Au] Autor:Yamamoto H; Sato H; Yagami K; Arikawa J; Furuya M; Kurosawa T; Mannen K; Matsubayashi K; Nishimune Y; Shibahara T; Ueda T; Itoh T
[Ad] Endereço:Laboratory Animal Research Center, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan.
[Ti] Título:Microbiological contamination in genetically modified animals and proposals for a microbiological test standard for national universities in Japan.
[So] Source:Exp Anim;50(5):397-407, 2001 Oct.
[Is] ISSN:1341-1357
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The Biosafety Committee of the Japanese Association of Laboratory Animal Facilities of National Universities (JALAN) investigated recent episodes of microbiological contamination in genetically modified mice (GMM), and the countermeasures taken when the contaminated GMM were introduced into animal facilities, by questionnaires addressed to 53 animal facilities belonging to JALAN and serological tests. Although almost all of the contaminated GMM were accepted with conditions such as rederivation after or before reception and housing in designated rooms, contamination with a spectrum of microorganisms was demonstrated in GMM transferred domestically and from abroad. In serological tests, Mycoplasma pulmonis, mouse parvovirus, and mouse encephalomylitis virus were detected in GMM transferred from domestic facilities and from abroad. The present results of the questionnaires and serological tests suggest that GMM are highly and widely contaminated with microorganisms compared with mice from commercial breeders. Thus, we propose a microbiological requirement, including microbiological status--excellent, common, and minimum--as a guide for the transfer and procurement of mice and rats in Japan.
[Mh] Termos MeSH primário: Transmissão de Doença Infecciosa/prevenção & controle
Controle de Infecções
Organismos Geneticamente Modificados/microbiologia
[Mh] Termos MeSH secundário: Animais
Guias como Assunto
Abrigo para Animais
Japão
Vírus Elberfeld do Camundongo/isolamento & purificação
Vírus Elberfeld do Camundongo/patogenicidade
Camundongos
Mycoplasma/isolamento & purificação
Mycoplasma/patogenicidade
Parvovirus/isolamento & purificação
Parvovirus/patogenicidade
Ratos
Medição de Risco
Testes Sorológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:0203
[Cu] Atualização por classe:161021
[Lr] Data última revisão:
161021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020105
[St] Status:MEDLINE



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