Base de dados : MEDLINE
Pesquisa : B04.613.807.375.525.050 [Categoria DeCS]
Referências encontradas : 652 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 66 ir para página                         

  1 / 652 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:16987061
[Au] Autor:Rich RF; Green WR
[Ad] Endereço:Department of Microbiology and Immunology and Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA.
[Ti] Título:Apoptosis of epitope-specific antiretroviral cytotoxic T lymphocytes via Fas ligand-Fas interactions.
[So] Source:Viral Immunol;19(3):424-33, 2006.
[Is] ISSN:0882-8245
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C57BL/6 (B6; H-2b) mice are capable of mounting a vigorous AKR/Gross Murine Leukemia Virus (MuLV)-specific cytotoxic T lymphocyte (CTL) response to AKR/Gross MuLVs whereas AKR.H- 2b congenic mice, although carrying the responder H-2b major histocompatibility haplotype, are specifically nonresponsive. Furthermore, when viable AKR.H-2b spleen cells are cocultured with primed responder B6 antiviral precursor CTLs, the AKR.H-2b cells function as "veto" cells that actively mediate the inhibition by apoptosis of B6 antiviral CTL generation in a contact-dependent, MHC-restricted, and veto cell Fas ligand (FasL)/responder T cell Fas-dependent manner. In the present study we show that antigen-specific, antiviral CTLs that survive apoptotic inhibition by AKR.H-2b veto cells display a less activated cell surface phenotype, and are less able to bind specific MHC-peptide tetramers, including on a per-T cell receptor (TcR) basis. In addition, surviving antiviral CTLs also appeared to be functionally deficient, based on both their reduced ability to lyse specific target cells and to produce interferon (IFN)-gamma. Carboxyfluorescein diacetate succinimidyl ester staining confirmed that AKR/Gross MuLV-specific CTLs proliferated less extensively when AKR.H-2b veto cells were included in cocultures. AKR/Gross MuLV-specific effector CTLs as well as memory CTLs were each efficiently targeted for inhibition by AKR.H-2b veto cells. Attempts to enhance the quality of the priming by multiple in vivo immunizations did not alter the capacity of the AKR.H-2b cells to inhibit the antiviral CTL response. These results further characterize the nature of the interaction between veto cells and antiviral CTLs, and underscore the efficiency of veto cell-mediated inhibition of the CTL response.
[Mh] Termos MeSH primário: Vírus AKR da Leucemia Murina/imunologia
Apoptose
Epitopos/imunologia
Proteína Ligante Fas/metabolismo
Linfócitos T Citotóxicos/fisiologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/patogenicidade
Animais
Linhagem Celular
Citotoxicidade Imunológica
Antígenos H-2
Masculino
Camundongos
Camundongos Congênicos
Camundongos Endogâmicos AKR
Camundongos Endogâmicos C57BL
Linfócitos T Citotóxicos/imunologia
Receptor fas/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 (Epitopes); 0 (Fas Ligand Protein); 0 (H-2 Antigens); 0 (fas Receptor)
[Em] Mês de entrada:0612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060922
[St] Status:MEDLINE


  2 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:16337984
[Au] Autor:Rich RF; Cook WJ; Green WR
[Ad] Endereço:Department of Microbiology and Immunology and the Norris Cotton Cancer Center, Dartmouth Medical School, 1 Medical Center Drive, Borwell 603 West, Lebanon, New Hampshire 03756, USA.
[Ti] Título:Spontaneous in vivo retrovirus-infected T and B cells, but not dendritic cells, mediate antigen-specific Fas ligand/Fas-dependent apoptosis of anti-retroviral CTL.
[So] Source:Virology;346(2):287-300, 2006 Mar 15.
[Is] ISSN:0042-6822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C57BL/6 (H-2b), but not spontaneous virus-expressing AKR.H-2b congenic, mice generate retrovirus-specific CD8+ CTL responses to the immunodominant Kb-restricted epitope, KSPWFTTL. AKR.H-2b non-responsiveness is mediated by a peripheral tolerance mechanism. When co-cultured with primed B6 antiviral pCTL, AKR.H-2b splenocytes are recognized by the antiviral TcR as "veto" cells, which inhibit by an exquisitely virus-specific, MHC-restricted, veto cell FasL/responder T cell Fas, mediated apoptotic mechanism. Here, AKR.H-2b thymus, lymph node, and bone marrow cells are also shown to inhibit antiviral CTL generation. Purified AKR.H-2b CD4+ and CD8+ T cells, and B cells, served effectively as FasL-dependent veto cells. In contrast, AKR.H-2b dendritic cells (DC) did not efficiently veto antiviral CTL responses, despite expressing sufficient MHC class I/viral peptide complexes for TcR recognition. AKR.H-2b DC also expressed FasL mRNA and cell surface protein, albeit at a lower level than AKR.H-2b T and B cells. These findings suggest a fail-safe escape mechanism by virus-infected cells for escape from CTL-mediated immunity.
[Mh] Termos MeSH primário: Apoptose
Linfócitos B/imunologia
Citotoxicidade Imunológica
Vírus da Leucemia Murina/imunologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/imunologia
Animais
Antígenos Virais/imunologia
Linfócitos B/virologia
Linhagem Celular
Células Cultivadas
Células Dendríticas/imunologia
Células Dendríticas/virologia
Proteína Ligante Fas
Citometria de Fluxo
Expressão Gênica
Antígenos H-2/imunologia
Masculino
Glicoproteínas de Membrana/fisiologia
Proteínas de Membrana/análise
Proteínas de Membrana/imunologia
Camundongos
RNA Mensageiro/análise
RNA Mensageiro/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Linfócitos T/virologia
Fatores de Necrose Tumoral/fisiologia
Receptor fas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Viral); 0 (Fas Ligand Protein); 0 (Fasl protein, mouse); 0 (H-2 Antigens); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (RNA, Messenger); 0 (Tumor Necrosis Factors); 0 (fas Receptor)
[Em] Mês de entrada:0604
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:051213
[St] Status:MEDLINE


  3 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:11884442
[Au] Autor:Rich RF; Green WR
[Ad] Endereço:Department of Microbiology and Immunology and The Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH 03756, USA.
[Ti] Título:Characterization of the Fas ligand/Fas-dependent apoptosis of antiretroviral, class I MHC tetramer-defined, CD8+ CTL by in vivo retrovirus-infected cells.
[So] Source:J Immunol;168(6):2751-8, 2002 Mar 15.
[Is] ISSN:0022-1767
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C57BL/6 (B6; H-2(b)) mice mount strong AKR/Gross murine leukemia virus (MuLV)-specific CD8(+) CTL responses to the immunodominant K(b)-restricted epitope, KSPWFTTL, of endogenous AKR/Gross MuLV. In sharp contrast, spontaneous virus-expressing AKR.H-2(b) congenic mice are low/nonresponders for the generation of AKR/Gross MuLV-specific CTL. Furthermore, when viable AKR.H-2(b) spleen cells are cocultured with primed responder B6 antiviral precursor CTL, the AKR.H-2(b) cells function as "veto" cells that actively mediate the inhibition of antiviral CTL generation. AKR.H-2(b) veto cell inhibition is virus specific, MHC restricted, contact dependent, and mediated through veto cell Fas ligand/responder T cell Fas interactions. In this study, following specific priming and secondary in vitro restimulation, antiretroviral CD8(+) CTL were identified by a labeled K(b)/KSPWFTTL tetramer and flow cytometry, enabling direct visualization of AKR.H-2(b) veto cell-mediated depletion of these CTL. A 65-93% reduction in the number of B6 K(b)/KSPWFTTL tetramer(+) CTL correlated with a similar reduction in antiviral CTL cytotoxicity. Addition on sequential days to the antiviral CTL restimulation cultures of either 1) AKR.H-2(b) veto cells or 2) a blocking Fas-Ig fusion protein (to cultures also containing AKR.H-2(b) veto cells) to block inhibition demonstrated that AKR.H-2(b) veto cells begin to inhibit B6 precursor CTL/CTL expansion during days 2 and 3 of the 6-day culture. Shortly thereafter, a high percentage of B6 tetramer(+) CTL cocultured with AKR.H-2(b) veto cells was annexin V positive and Fas(high), indicating apoptosis as the mechanism of veto cell inhibition. Experiments using the irreversible inhibitor emetine demonstrated that AKR.H-2(b) cells had to be metabolically active and capable of protein synthesis to function as veto cells. Of the tetramer-positive CTL that survived veto cell-mediated apoptosis, there was no marked skewing from the preferential usage of Vbeta4, 8.1/8.2, and 11 TCR normally observed. These findings provide further insight into the complexity of host/virus interactions and suggest a fail-safe escape mechanism by virus-infected cells for epitopes residing in critical areas of viral proteins that cannot accommodate variations of amino acid sequence.
[Mh] Termos MeSH primário: Vírus AKR da Leucemia Murina/imunologia
Apoptose/imunologia
Citotoxicidade Imunológica
Antígenos H-2/análise
Glicoproteínas de Membrana/fisiologia
Subpopulações de Linfócitos T/virologia
Linfócitos T Citotóxicos/virologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/crescimento & desenvolvimento
Animais
Divisão Celular/imunologia
Deleção Clonal
Epitopos de Linfócito T/análise
Epitopos de Linfócito T/imunologia
Proteína Ligante Fas
Inibidores do Crescimento/biossíntese
Inibidores do Crescimento/fisiologia
Receptores de Hialuronatos/biossíntese
Cinética
Ligantes
Ativação Linfocitária
Contagem de Linfócitos
Camundongos
Camundongos Endogâmicos AKR
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Fragmentos de Peptídeos/biossíntese
Fragmentos de Peptídeos/imunologia
Receptores de Antígenos de Linfócitos T alfa-beta/biossíntese
Subpopulações de Linfócitos T/citologia
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Citotóxicos/citologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
Células Tumorais Cultivadas
Receptor fas/biossíntese
Receptor fas/metabolismo
Receptor fas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Epitopes, T-Lymphocyte); 0 (Fas Ligand Protein); 0 (Fasl protein, mouse); 0 (Growth Inhibitors); 0 (H-2 Antigens); 0 (H-2Kb protein, mouse); 0 (Hyaluronan Receptors); 0 (Ligands); 0 (Membrane Glycoproteins); 0 (Peptide Fragments); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (fas Receptor)
[Em] Mês de entrada:0204
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:020309
[St] Status:MEDLINE


  4 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:10775791
[Au] Autor:Galvin TA; Muller J; Khan AS
[Ad] Endereço:Laboratory of Retrovirus Research, Center for Biologics Evaluation and Research, US Food and Drug Administration, Bethesda, MD 20892, USA.
[Ti] Título:Effect of different promoters on immune responses elicited by HIV-1 gag/env multigenic DNA vaccine in Macaca mulatta and Macaca nemestrina.
[So] Source:Vaccine;18(23):2566-83, 2000 May 22.
[Is] ISSN:0264-410X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:pCMV-NL(Deltapol) and pAKV-NL(Deltapol) expressed human immunodeficiency virus type 1 (HIV-1) gag and env under the regulation of the human cytomegalovirus (CMV) immediate-early (IE) promoter/enhancer and the endogenous AKV murine leukemia viral long terminal repeat (LTR), respectively. Analysis of the immune responses elicited by direct DNA injection of pCMV-NL(Deltapol) and pAKV-NL(Deltapol) in macaques indicated that generation of the humoral and T-cell proliferative responses correlated directly with the promoter strength of the vaccine DNAs. In Macaca mulatta, pCMV-NL(Deltapol) generated stronger humoral responses and T-cell proliferative responses to Gag and Env using less DNA and fewer number of injections than pAKV-NL(Deltapol). Similarly, in Macaca nemestrina pCMV-NL(Deltapol) elicited high humoral responses, which persisted long-term and were boostable. Injection of large amounts of pAKV-NL(Deltapol), in general, failed to produce antibody levels comparable to pCMV-NL(Deltapol). However, injection of a control animal with large amounts of vector DNA produced a generalized enzyme-linked immunosorbent assay (ELISA) reactivity to HIV-1. The results indicated that generation of high immune responses to HIV-1 cannot be achieved by increasing the vaccine DNA dose and may require high protein expression from the DNA by including a strong promoter or by the use of other boosting agents. Furthermore, safety concerns may arise with increasing the DNA dose that could need additional investigation.
[Mh] Termos MeSH primário: Vacinas contra a AIDS/imunologia
Vírus AKR da Leucemia Murina/genética
Antígenos Virais/genética
Citomegalovirus/genética
Genes Virais
Genes env
Genes gag
Proteína do Núcleo p24 do HIV/imunologia
Proteína gp120 do Envelope de HIV/imunologia
Proteína gp41 do Envelope de HIV/imunologia
HIV-1/imunologia
Proteínas Imediatamente Precoces/genética
Regiões Promotoras Genéticas
Sequências Repetidas Terminais
Vacinas de DNA/imunologia
[Mh] Termos MeSH secundário: Células 3T3
Animais
Sequência de Bases
Cercopithecus aethiops
Cloranfenicol O-Acetiltransferase/análise
Elementos Facilitadores Genéticos/genética
Genes Reporter
Anticorpos Anti-HIV/biossíntese
Anticorpos Anti-HIV/imunologia
Proteína do Núcleo p24 do HIV/biossíntese
Proteína gp120 do Envelope de HIV/biossíntese
Proteína gp160 do Envelope de HIV/biossíntese
Proteína gp160 do Envelope de HIV/imunologia
Proteína gp41 do Envelope de HIV/biossíntese
HIV-1/genética
Seres Humanos
Ativação Linfocitária
Macaca mulatta
Macaca nemestrina
Camundongos
Dados de Sequência Molecular
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Rabdomiossarcoma/patologia
Segurança
Especificidade da Espécie
Linfócitos T Citotóxicos/imunologia
Transfecção
Células Vero
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIDS Vaccines); 0 (Antigens, Viral); 0 (HIV Antibodies); 0 (HIV Core Protein p24); 0 (HIV Envelope Protein gp120); 0 (HIV Envelope Protein gp160); 0 (HIV Envelope Protein gp41); 0 (Immediate-Early Proteins); 0 (Recombinant Fusion Proteins); 0 (Vaccines, DNA); 0 (immediate-early proteins, cytomegalovirus); EC 2.3.1.28 (Chloramphenicol O-Acetyltransferase)
[Em] Mês de entrada:0008
[Cu] Atualização por classe:081121
[Lr] Data última revisão:
081121
[Sb] Subgrupo de revista:IM; X
[Da] Data de entrada para processamento:000425
[St] Status:MEDLINE


  5 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
[PMID]:10623721
[Au] Autor:Mikkelsen JG; Lund AH; Duch M; Pedersen FS
[Ad] Endereço:Department of Molecular and Structural Biology, University of Aarhus, DK-8000 Aarhus, Denmark.
[Ti] Título:Mutations of the kissing-loop dimerization sequence influence the site specificity of murine leukemia virus recombination in vivo.
[So] Source:J Virol;74(2):600-10, 2000 Jan.
[Is] ISSN:0022-538X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The genetic information of retroviruses is retained within a dimeric RNA genome held together by intermolecular RNA-RNA interactions near the 5' ends. Coencapsidation of retrovirus-derived RNA molecules allows frequent template switching of the virus-encoded reverse transcriptase during DNA synthesis in newly infected cells. We have previously shown that template shifts within the 5' leader of murine leukemia viruses occur preferentially within the kissing stem-loop motif, a cis element crucial for in vitro RNA dimer formation. By use of a forced recombination approach based on single-cycle transfer of Akv murine leukemia virus-based vectors harboring defective primer binding site sequences, we now report that modifications of the kissing-loop structure, ranging from a deletion of the entire sequence to introduction of a single point mutation in the loop motif, significantly disturb site specificity of recombination within the highly structured 5' leader region. In addition, we find that an intact kissing-loop sequence favors optimal RNA encapsidation and vector transduction. Our data are consistent with the kissing-loop dimerization model and suggest that a direct intermolecular RNA-RNA interaction, here mediated by palindromic loop sequences within the mature genomic RNA dimer, facilitates hotspot template switching during retroviral cDNA synthesis in vivo.
[Mh] Termos MeSH primário: Vírus da Leucemia Murina/genética
RNA Viral/metabolismo
Recombinação Genética
[Mh] Termos MeSH secundário: Células 3T3
Regiões 5' não Traduzidas
Vírus AKR da Leucemia Murina/genética
Vírus AKR da Leucemia Murina/fisiologia
Animais
Sequência de Bases
Sítios de Ligação
DNA Viral
Dimerização
Vírus da Leucemia Murina/fisiologia
Camundongos
Dados de Sequência Molecular
Mutagênese
RNA
RNA Viral/genética
Análise de Sequência de RNA
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (DNA, Viral); 0 (RNA primers); 0 (RNA, Viral); 63231-63-0 (RNA)
[Em] Mês de entrada:0002
[Cu] Atualização por classe:140615
[Lr] Data última revisão:
140615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:000107
[St] Status:MEDLINE


  6 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:10551449
[Au] Autor:Hesse I; Luz A; Kohleisen B; Erfle V; Schmidt J
[Ad] Endereço:Institute of Molecular Virology, GSF-National Research Center for Environment and Health, Neuherberg, Germany.
[Ti] Título:Prenatal transmission and pathogenicity of endogenous ecotropic murine leukemia virus Akv.
[So] Source:Lab Anim Sci;49(5):488-95, 1999 Oct.
[Is] ISSN:0023-6764
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Mouse strains carrying endogenous ecotropic murine leukemia viruses (MuLV) are capable of expressing infective virus throughout life. Risk of transplacental transmission of MuLV raises concerns of embryo infection and induction of pathogenic effects, and postnatal MuLV infection may lead to tumorigenesis. METHODS: Endogenous ecotropic MuLV-negative SWR/J embryos were implanted into Akv-infected viremic SWR/J mice, into spontaneously provirus-expressing AKR/J mice, and into noninfected SWR/J control mice; virus integration and virus expression were investigated at 14 days' gestation. Tumor development was monitored over 18 months. RESULTS: Of 111 embryos, 20 (18%) recovered from Akv-infected SWR/J mice, which had developed normally, were infected. New proviruses were detected in 10 of 111 (9%) embryos from Akv-infected SWR/J mice, and in 2 of 60 (3%) embryos from AKR/J mice; none expressed viral protein. Of 127 embryos recovered from Akv-infected SWR/J mice, 16 (13%) were dead; 4 of 5 (80%) were infected and expressed viral protein. Of 71 embryos from AKR/J mice, 11 (15%) were dead, and 2 of 2 had virus integration; virus expression was not detected. Numbers of dead embryos recovered from experimentally infected, viremic SWR/J mice and from spontaneously endogenous MuLV-expressing AKR/J mice were significantly higher, compared with numbers from nonviremic SWR/J control mice, and embryo lethality was significantly associated with prenatal provirus expression. Postnatal inoculation of Akv induced lymphoblastic lymphomas in 15 of 24 (61%) SWR/J mice within mean +/- SD latency of 14 +/- 2.4 months. Only 3 of 39 (8%) control mice developed lymphomas (P < 0.005). CONCLUSION: Embryos in MuLV-viremic dams are readily infected, and inappropriate prenatal expression of leukemogenic endogenous retroviruses may play a critical role in embryo lethality and decreased breeding performance in ecotropic provirus-positive mouse strains.
[Mh] Termos MeSH primário: Vírus AKR da Leucemia Murina/patogenicidade
Transmissão Vertical de Doença Infecciosa
Leucemia/veterinária
Infecções por Retroviridae/veterinária
Doenças dos Roedores/virologia
Infecções Tumorais por Vírus/veterinária
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/genética
Animais
Animais Recém-Nascidos/virologia
DNA Viral/análise
Transferência Embrionária
Embrião de Mamíferos/virologia
Feminino
Morte Fetal/virologia
Idade Gestacional
Leucemia/virologia
Camundongos
Gravidez
Infecções por Retroviridae/transmissão
Doenças dos Roedores/transmissão
Infecções Tumorais por Vírus/transmissão
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Viral)
[Em] Mês de entrada:9912
[Cu] Atualização por classe:081121
[Lr] Data última revisão:
081121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:991107
[St] Status:MEDLINE


  7 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
[PMID]:10196277
[Au] Autor:Rich RF; Green WR
[Ad] Endereço:Department of Microbiology and the Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA.
[Ti] Título:Antiretroviral cytolytic T-lymphocyte nonresponsiveness: FasL/Fas-mediated inhibition of CD4(+) and CD8(+) antiviral T cells by viral antigen-positive veto cells.
[So] Source:J Virol;73(5):3826-34, 1999 May.
[Is] ISSN:0022-538X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C57BL/6 (H-2(b)) mice generate type-specific cytolytic T-lymphocyte (CTL) responses to an immunodominant Kb-restricted epitope, KSPWFTTL located in the membrane-spanning domain of p15TM of AKR/Gross murine leukemia viruses (MuLV). AKR.H-2(b) congenic mice, although carrying the responder H-2(b) major histocompatibility complex (MHC) haplotype, are low responders or nonresponders for AKR/Gross MuLV-specific CTL, apparently due to the presence of inhibitory AKR. H-2(b) cells. Despite their expression of viral antigens and Kb, untreated viable AKR.H-2(b) spleen cells cause dramatic inhibition of the C57BL/6 (B6) antiviral CTL response to in vitro stimulation with AKR/Gross MuLV-induced tumor cells. This inhibition is specific (AKR.H-2(b) modulator spleen cells do not inhibit allogeneic MHC or minor histocompatibility antigen-specific CTL production), dependent on direct contact of AKR.H-2(b) cells in a dose-dependent manner with the responder cell population, and not due to soluble factors. Here, the mechanism of inhibition of the antiviral CTL response is shown to depend on Fas/Fas-ligand interactions, implying an apoptotic effect on B6 responder cells. Although B6.gld (FasL-) responders were as sensitive to inhibition by AKR.H-2(b) modulator cells as were B6 responders, B6.lpr (Fas-) responders were largely insensitive to inhibition, indicating that the responder cells needed to express Fas. A Fas-Ig fusion protein, when added to the in vitro CTL stimulation cultures, relieved the inhibition caused by the AKR.H-2(b) cells if the primed responders were from either B6 or B6.gld mice, indicating that the inhibitory AKR.H-2(b) cells express FasL. Because of the antigen specificity of the inhibition, these results collectively implicate a FasL/Fas interaction mechanism: viral antigen-positive AKR.H-2(b) cells expressing FasL inhibit antiviral T cells ("veto" them) when the AKR.H-2(b) cells are recognized. Consistent with this model, inhibition by AKR.H-2(b) modulator cells was MHC restricted, and resulted in approximately a 10- to 70-fold decrease in the in vitro expansion of pCTL/CTL. Both CD8(+) CTL and CD4(+) Th responder cells were susceptible to inhibition by FasL+ AKR.H-2(b) inhibitory cells as the basis for inhibition. The CTL response in the presence of inhibitory cells could be restored by several cytokines or agents that have been shown by others to interfere with activation-induced cell death (e.g. , interleukin-2 [IL-2], IL-15, transforming growth factor beta, lipopolysaccharide, 9-cis-retinoic acid) but not others (e.g., tumor necrosis factor alpha). These results raise the possibility that this type of inhibitory mechanism is generalized as a common strategy for retrovirus infected cells to evade immune T-cell recognition.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Glicoproteínas de Membrana/imunologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/virologia
Receptor fas/imunologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina
Animais
Proteína Ligante Fas
Feminino
Antígenos H-2/imunologia
Seres Humanos
Interleucina-15/imunologia
Lipopolissacarídeos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Recombinantes de Fusão/imunologia
Baço/citologia
Fator de Crescimento Transformador beta/imunologia
Tretinoína
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (Fasl protein, mouse); 0 (H-2 Antigens); 0 (Interleukin-15); 0 (Lipopolysaccharides); 0 (Membrane Glycoproteins); 0 (Recombinant Fusion Proteins); 0 (Transforming Growth Factor beta); 0 (Tumor Necrosis Factor-alpha); 0 (fas Receptor); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:9905
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM; X
[Da] Data de entrada para processamento:990410
[St] Status:MEDLINE


  8 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:10189187
[Au] Autor:Kim V; Green WR
[Ad] Endereço:Department of Microbiology, Dartmouth Medical School and The Norris Cotton Cancer Center, Lebanon, New Hampshire 03756, USA.
[Ti] Título:A single amino acid variation within an immunodominant AKR/Gross MuLV cytotoxic T-lymphocyte epitope leads to a loss in immunogenicity.
[So] Source:Viral Immunol;11(4):197-213, 1998.
[Is] ISSN:0882-8245
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:C57BL/6 mice characteristically generate vigorous H-2K(b)-restricted cytotoxic T lymphocytes (CTL) directed against an immunodominant CTL epitope (KSPWFTTL) expressed by endogenous AKR/Gross murine leukemia viruses (MuLV). These AKR/Gross MuLV-specific CTL do not efficiently recognize tumor cells induced by Friend/Moloney/Rauscher (FMR) MuLV, which express the highly homologous peptide RSPWFTTL. In this report, we not only confirm the inefficient recognition of FMR tumors by AKR/Gross MuLV-specific CTL, but also demonstrate that RSPWFTTL is poorly immunogenic in C57BL/6 mice. To gain insight into the mechanism(s) contributing to the inefficient recognition of FMR MuLV-induced tumors, we examined the RSPWFTTL dissociation rate from H-2K(b) as well as the ability for RSPWFTTL to diminish CTL effector functions by T-cell antagonism. In contrast to immunogenic peptides, which form stable MHC class I-peptide complexes having slow dissociation rates, poorly immunogenic peptides characteristically have faster dissociation rates. On the basis of a cell-surface MHC class I peptide stabilization assay, the dissociation rate of RSP-WFTTL from H-2K(b) is characterized by a half-life that is nearly identical to the half-life of KSPWFTTL. In addition, we could find no evidence for antagonistic inhibition of AKR/Gross MuLV-specific CTL over a wide concentration range of RSPWFTTL. Analysis of the role of the transporter associated with antigen processing (TAP), by use of recombinant vaccinia and Sindbis viruses expressing a hydrophobic amino-terminal endoplasmic reticulum (ER) targeting sequence coupled to RSPWFTTL, indicated that RSPWFTTL cell-surface presentation can be dramatically enhanced when directly targeted into the ER.
[Mh] Termos MeSH primário: Vírus AKR da Leucemia Murina/imunologia
Substituição de Aminoácidos
Epitopos de Linfócito T/imunologia
Variação Genética
Epitopos Imunodominantes/imunologia
Linfócitos T Citotóxicos/imunologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/genética
Membro 2 da Subfamília B de Cassetes de Ligação de ATP
Transportadores de Cassetes de Ligação de ATP/imunologia
Sequência de Aminoácidos
Animais
Linhagem Celular
Epitopos de Linfócito T/genética
Feminino
Antígenos H-2/imunologia
Epitopos Imunodominantes/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Dados de Sequência Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (ATP-Binding Cassette Sub-Family B Member 2); 0 (Epitopes, T-Lymphocyte); 0 (H-2 Antigens); 0 (H-2Kb protein, mouse); 0 (Immunodominant Epitopes); 0 (TAP1 protein, human); 0 (Tap1 protein, mouse)
[Em] Mês de entrada:9905
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:990403
[St] Status:MEDLINE


  9 / 652 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:9393630
[Au] Autor:Lindvall M; Eriksson H; Hedlund G; Sjögren HO
[Ad] Endereço:Department of Tumor Immunology, Wallenberg Laboratory, Lund University.
[Ti] Título:Selective cytotoxicity of two rodent T cell lymphomas to rat yolk sac tumours involves a retroviral envelope protein expressed by the lymphoma.
[So] Source:Scand J Immunol;46(5):479-87, 1997 Nov.
[Is] ISSN:0300-9475
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A Gross virus induced rat T cell lymphoma G1-Tc1 and a Moloney virus induced mouse T cell lymphoma YAC-1 are shown to exert a strong cytotoxic activity against rat yolk sac tumours but not to various types of rat, mouse or human normal cells or tumour cell lines including carcinomas, sarcomas, lymphomas and gliomas. Both lymphomas are CD3+, CD4-, CD8- and T-cell receptor (TCR) alpha beta +. The cytotoxicity was not MHC restricted or dependent on the density of MHC class I of the target cells, and the mouse lymphoma killed the rat yolk sac tumour target. The cytotoxic action was fast and up to 80% specific killing was observed in 4-h 51Cr release assays. A rat B cell hybridoma was established from a Wistar/Furth (WF) rat immunized with the syngeneic lymphoma G1-Tc1 producing an immunoglobulin (Ig)G2c monoclonal antibody (MoAb) 1F2. This binds to the lymphomas G1-Tc1 and YAC-1 and also to a murine non-cytolytic Rauscher lymphoma RMA, but not to any other of several rat, mouse or human cell types tested. The 1F2 completely inhibited the killing of rat yolk sac tumours by the two cytolytic lymphomas, but did not interfere with the killing mediated by natural killer (NK) cells or cytolytic lymphokine-activated killer (LAK) cells. Immunochemical analysis of solubilized cell membranes of the lymphoma G1-Tc1 demonstrates that the 1F2 antibody recognizes an epitope on a retroviral gp 70 envelope protein. This indicates that a retroviral protein is involved in the lytic activity of the two lymphomas.
[Mh] Termos MeSH primário: Vírus AKR da Leucemia Murina/fisiologia
Citotoxicidade Imunológica
Tumor do Seio Endodérmico/imunologia
Linfoma de Células T/imunologia
Proteínas de Membrana/fisiologia
Vírus da Leucemia Murina de Moloney/fisiologia
Proteínas de Neoplasias/fisiologia
Células-Tronco Neoplásicas/imunologia
Proteínas Oncogênicas de Retroviridae/fisiologia
Proteínas do Envelope Viral/fisiologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/genética
Vírus AKR da Leucemia Murina/imunologia
Animais
Anticorpos Monoclonais/imunologia
Anticorpos Monoclonais/farmacologia
Linhagem Celular
Citotoxicidade Imunológica/efeitos dos fármacos
Epitopos/imunologia
Seres Humanos
Linfoma de Células T/virologia
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Camundongos
Vírus da Leucemia Murina de Moloney/genética
Vírus da Leucemia Murina de Moloney/imunologia
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/imunologia
Ratos
Ratos Endogâmicos WF
Proteínas Oncogênicas de Retroviridae/genética
Proteínas Oncogênicas de Retroviridae/imunologia
Proteínas do Envelope Viral/genética
Proteínas do Envelope Viral/imunologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Epitopes); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (Retroviridae Proteins, Oncogenic); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:9712
[Cu] Atualização por classe:071115
[Lr] Data última revisão:
071115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:971211
[St] Status:MEDLINE


  10 / 652 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:9325230
[Au] Autor:Kim V; Green WR
[Ad] Endereço:Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire, USA.
[Ti] Título:The role of proximal and distal sequence variations in the presentation of an immunodominant CTL epitope encoded by the ecotropic AK7 MuLV.
[So] Source:Virology;236(2):221-33, 1997 Sep 29.
[Is] ISSN:0042-6822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An emv-14-derived, replication-competent ecotropic murine leukemia virus [MuLV], designated AK7, was previously cloned from the AKXL-5 recombinant inbred mouse strain and partially characterized. While genetically encoding for an envelope-derived immunodominant CTL epitope [KSPWFTTL] located in the transmembrane region of p15TM, this virus, unlike the emv-11-derived virus AKR623, fails to be efficiently recognized by AKR/Gross MuLV-specific cytotoxic T lymphocytes [CTL]. AK7 thus provides the opportunity to study the role of retroviral sequence variations that are located outside of the immunodominant epitope as a mechanism of escape from CTL-mediated immune surveillance. In an attempt to identify which region[s] of the AK7 genome could account for its ability to evade efficient recognition by AKR/Gross MuLV-specific CTL, we have constructed recombinant murine retroviruses. The direct influence of a sequence variation twelve amino acids N-terminal to KSPWFTTL was explored with the use of chimeric viruses and determined not to significantly impair the presentation of KSPWFTTL to AKR/Gross MuLV-specific CTL. The long terminal repeat [LTR] derived from the AK7 virus, which possesses only one copy of the 99-base pair transcriptional enhancer in the U3 region, in contrast to AKR623 that possesses two copies of the tandem direct repeat enhancers, was also analyzed for its influence on the presentation of KSPWFTTL. Interestingly, our data indicate that the enhancer region derived from AK7 negatively influences the presentation of KSPWFTTL in the context of a recombinant AKR623 virus.
[Mh] Termos MeSH primário: Variação Antigênica
Antígenos Virais/genética
Vírus da Leucemia Murina/genética
Vírus da Leucemia Murina/imunologia
[Mh] Termos MeSH secundário: Vírus AKR da Leucemia Murina/genética
Vírus AKR da Leucemia Murina/imunologia
Sequência de Aminoácidos
Animais
Apresentação do Antígeno
Sequência de Bases
Linhagem Celular
Primers do DNA/genética
Elementos Facilitadores Genéticos
Epitopos Imunodominantes/genética
Camundongos
Dados de Sequência Molecular
Reação em Cadeia da Polimerase
Homologia de Sequência de Aminoácidos
Linfócitos T Citotóxicos/imunologia
Proteínas do Envelope Viral/genética
Proteínas do Envelope Viral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antigens, Viral); 0 (DNA Primers); 0 (Immunodominant Epitopes); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:9711
[Cu] Atualização por classe:081121
[Lr] Data última revisão:
081121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:971105
[St] Status:MEDLINE



página 1 de 66 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