Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.852.760.500 [Categoria DeCS]
Referências encontradas : 319 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 32 ir para página                         

  1 / 319 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28470686
[Au] Autor:Sideras K; Biermann K; Yap K; Mancham S; Boor PPC; Hansen BE; Stoop HJA; Peppelenbosch MP; van Eijck CH; Sleijfer S; Kwekkeboom J; Bruno MJ
[Ad] Endereço:Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center, Rotterdam, The Netherlands.
[Ti] Título:Tumor cell expression of immune inhibitory molecules and tumor-infiltrating lymphocyte count predict cancer-specific survival in pancreatic and ampullary cancer.
[So] Source:Int J Cancer;141(3):572-582, 2017 08 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Understanding the mechanisms of immune resistance in pancreatic and ampullary cancers is crucial for the development of suitable biomarkers and effective immunotherapeutics. Our aim was to examine the expression of the immune inhibiting molecules PD-L1, Galectin-9, HVEM, IDO and HLA-G, as well as CD8+ and FoxP3+ tumor infiltrating lymphocytes (TIL), in pancreatic and ampullary cancers, and to relate their individual, as well as their combined expression, to cancer survival. Tumor tissue from 224 patients with resected pancreatic (n = 148) and ampullary (n = 76) cancer was used to construct tissue-microarrays. Expression of immune inhibitory molecules and TIL was examined by immunohistochemistry. We show that immune inhibitory molecules are prevalently expressed. Moreover, high tumor expression of PD-L1 (p = 0.002), Gal-9 (p = 0.003), HVEM (p = 0.001), IDO (p = 0.049), HLA-G (p = 0.004) and high CD8/FoxP3 TIL ratio (p = 0.006) were associated with improved cancer-specific survival. All immune biomarkers, with the exception of IDO, were individually predictive of cancer-specific survival when adjusted for clinicopathologic characteristics. For every additional immune biomarker present survival was almost two-fold prolonged (HR 0.57 95%CI 0.47-0.69, p < 0.0001). When patients with pancreatic and ampullary cancer were analyzed separately the results were similar. We conclude that pancreas and ampullary cancers are rich in expression of immune-inhibitory molecules. These molecules can be targets for future immunotherapeutics, as well as form powerful immunological biomarkers. We propose that such immune biomarker panels be included in future prospective immunotherapy trials.
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Neoplasias do Ducto Colédoco/mortalidade
Galanina/metabolismo
Antígenos HLA-G/metabolismo
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Linfócitos do Interstício Tumoral/imunologia
Neoplasias Pancreáticas/mortalidade
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Ampola Hepatopancreática/imunologia
Ampola Hepatopancreática/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias do Ducto Colédoco/imunologia
Neoplasias do Ducto Colédoco/metabolismo
Feminino
Seres Humanos
Linfócitos do Interstício Tumoral/metabolismo
Linfócitos do Interstício Tumoral/patologia
Masculino
Meia-Idade
Neoplasias Pancreáticas/imunologia
Neoplasias Pancreáticas/metabolismo
Prognóstico
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD274 protein, human); 0 (GAL protein, human); 0 (HLA-G Antigens); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (TNFRSF14 protein, human); 88813-36-9 (Galanin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30760


  2 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28422285
[Au] Autor:Chen W; Lv X; Liu C; Chen R; Liu J; Dai H; Zou GM
[Ad] Endereço:Xinhua Hospital, Shanghai Institute of Pediatric Research, Shanghai, China.
[Ti] Título:Hematopoietic stem/progenitor cell differentiation towards myeloid lineage is modulated by LIGHT/LIGHT receptor signaling.
[So] Source:J Cell Physiol;233(2):1095-1103, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytokine LT-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells (LIGHT) is a member of the tumor necrosis factor (TNF) superfamily. It is expressed primarily on activated T lymphocytes, and detectable on monocytes, granulocytes, and immune dendritic cells. It mainly plays a role in immune regulation including T cell activation and dendritic cell maturation. We recently reported its role as an inducer in embryonic stem cell differentiation, but its role in regulation of adult stem cell has not been defined. In the present study, we examined the expression of LIGHT receptor in Lin c-kit Sca-1 hematopoietic stem/progenitor cells (HSC/HPCs). We found that HSC express HVEM, a LIGHT receptor, on its surface. We further identified the role of LIGHT in promoting myeloid differentiation of HSCs driven by granulocyte-monocyte colony stimulating factor (GM-CSF). Further studies showed that LIGHT enhances both GM-CSF and GM-CSF receptor (GM-CSFR) expression in HSCs. LIGHT stimulation increases PU.1 expression in HSC/HPCs. In vivo administration of LIGHT increases the colony-forming unit-granulocyte/monocyte (CFU-GM) colony formation and plasma GM-CSF level. Altogether, the data suggest LIGHT promote myeloid differentiation of HSC/HPCs.
[Mh] Termos MeSH primário: Diferenciação Celular
Linhagem da Célula
Células-Tronco Hematopoéticas/metabolismo
Células Mieloides/metabolismo
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/metabolismo
Proliferação Celular
Células Cultivadas
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Masculino
Proteínas de Membrana/metabolismo
Camundongos Endogâmicos C57BL
Fenótipo
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/metabolismo
Transativadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Ly6a protein, mouse); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Tnfrsf14 protein, mouse); 0 (Tnfsf14 protein, mouse); 0 (Trans-Activators); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (proto-oncogene protein Spi-1); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25967


  3 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28864473
[Au] Autor:Desai P; Abboud G; Stanfield J; Thomas PG; Song J; Ware CF; Croft M; Salek-Ardakani S
[Ad] Endereço:Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32603.
[Ti] Título:HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity.
[So] Source:J Immunol;199(8):2968-2975, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mucosal immunity to reinfection with a highly virulent virus requires the accumulation and persistence of memory CD8 T cells at the site of primary infection. These cells may derive from memory precursor effector cells (MPECs), which are distinct from short-lived effector cells that provide acute protection but are often destined to die. Using respiratory virus infection, we show that herpes virus entry mediator (HVEM; TNFRSF14), a member of the TNF receptor superfamily, provides key signals for MPEC persistence. HVEM-deficient CD8 T cells expanded normally but were skewed away from MPECs with resultant poor development of circulating and lung-resident memory cells. HVEM was selectively expressed on MPECs whereas MPECs deficient in HVEM failed to survive in adoptive transfer recipients. As a consequence, HVEM-deficient recipients failed to afford protection against respiratory reinfection with influenza virus. HVEM therefore represents a critical signal for MPECs and development of protective mucosal CD8 T cell memory.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Vírus da Influenza A/imunologia
Infecções por Orthomyxoviridae/imunologia
Células Precursoras de Linfócitos T/imunologia
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos T CD8-Positivos/virologia
Autorrenovação Celular
Células Cultivadas
Modelos Animais de Doenças
Feminino
Imunidade nas Mucosas
Memória Imunológica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Células Precursoras de Linfócitos T/virologia
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Tnfrsf14 protein, mouse)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700959


  4 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28809154
[Au] Autor:Hu K; He S; Xiao J; Li M; Luo S; Zhang M; Hu Q
[Ad] Endereço:2​Institute for Infection and Immunity, St George's University of London, London SW17 0RE, UK 1​State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, PR China.
[Ti] Título:Interaction between herpesvirus entry mediator and HSV-2 glycoproteins mediates HIV-1 entry of HSV-2-infected epithelial cells.
[So] Source:J Gen Virol;98(9):2351-2361, 2017 Sep.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Herpes simplex virus type 2 (HSV-2) increases human immunodeficiency virus type 1 (HIV-1) acquisition and transmission via unclear mechanisms. Herpesvirus entry mediator (HVEM), an HSV-2 entry receptor, is highly expressed on HIV-1 target cells (CD4+ T cells) and may be incorporated into HIV-1 virions, while HSV-2 glycoproteins can be present on the infected cell surface. Since HVEM-gD interaction together with gB/gH/gL is essential for HSV-2 entry, HVEM-bearing HIV-1 (HIV-1/HVEM) may enter HSV-2-infected cells through such interactions. To test this hypothesis, we first confirmed the presence of HVEM on HIV-1 virions and glycoproteins on the HSV-2-infected cell surface. Additional studies showed that HIV-1/HVEM bound to the HSV-2-infected cell surface in an HSV-2 infection-time-dependent manner via HVEM-gD interaction. HIV-1/HVEM entry of HSV-2-infected cells was dependent on HVEM-gD interaction and the presence of gB/gH/gL, and was inhibited by azidothymidine. Furthermore, peripheral blood mononuclear cell-derived HIV-1 infected HSV-2-infected primary foreskin epithelial cells and the infection was inhibited by anti-HVEM/gD antibodies. Together, our results indicate that HIV-1 produced from CD4+ T cells bears HSV-2 receptor HVEM and can bind to and enter HSV-2-infected epithelial cells depending on HVEM-gD interaction and the presence of gB/gH/gL. Our findings provide a potential new mechanism underlying HSV-2 infection-enhanced HIV-1 mucosal transmission and may shed light on HIV-1 prevention.
[Mh] Termos MeSH primário: Células Epiteliais/metabolismo
Infecções por HIV/metabolismo
HIV-1/fisiologia
Herpes Simples/metabolismo
Herpesvirus Humano 2/fisiologia
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
Receptores Virais/metabolismo
Proteínas do Envelope Viral/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/virologia
Células CHO
Cricetulus
Células Epiteliais/virologia
Infecções por HIV/genética
Infecções por HIV/virologia
HIV-1/genética
Herpes Simples/genética
Herpesvirus Humano 2/genética
Seres Humanos
Camundongos
Ligação Proteica
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
Receptores Virais/genética
Proteínas do Envelope Viral/genética
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Receptors, Virus); 0 (Viral Envelope Proteins); 0 (glycoprotein B, herpes simplex virus type 2); 0 (glycoprotein D-herpes simplex virus type 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000895


  5 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28701403
[Au] Autor:Wang K; Tomaras GD; Jegaskanda S; Moody MA; Liao HX; Goodman KN; Berman PW; Rerks-Ngarm S; Pitisuttithum P; Nitayapan S; Kaewkungwal J; Haynes BF; Cohen JI
[Ad] Endereço:Medical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
[Ti] Título:Monoclonal Antibodies, Derived from Humans Vaccinated with the RV144 HIV Vaccine Containing the HVEM Binding Domain of Herpes Simplex Virus (HSV) Glycoprotein D, Neutralize HSV Infection, Mediate Antibody-Dependent Cellular Cytotoxicity, and Protect Mice from Ocular Challenge with HSV-1.
[So] Source:J Virol;91(19), 2017 Oct 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The RV144 HIV vaccine trial included a recombinant HIV glycoprotein 120 (gp120) construct fused to a small portion of herpes simplex virus 1 (HSV-1) glycoprotein D (gD) so that the first 40 amino acids of gp120 were replaced by the signal sequence and the first 27 amino acids of the mature form of gD. This region of gD contains most of the binding site for HVEM, an HSV receptor important for virus infection of epithelial cells and lymphocytes. RV144 induced antibodies to HIV that were partially protective against infection, as well as antibodies to HSV. We derived monoclonal antibodies (MAbs) from peripheral blood B cells of recipients of the RV144 HIV vaccine and showed that these antibodies neutralized HSV-1 infection in cells expressing HVEM, but not the other major virus receptor, nectin-1. The MAbs mediated antibody-dependent cellular cytotoxicity (ADCC), and mice that received the MAbs and were then challenged by corneal inoculation with HSV-1 had reduced eye disease, shedding, and latent infection. To our knowledge, this is the first description of MAbs derived from human recipients of a vaccine that specifically target the HVEM binding site of gD. In summary, we found that monoclonal antibodies derived from humans vaccinated with the HVEM binding domain of HSV-1 gD (i) neutralized HSV-1 infection in a cell receptor-specific manner, (ii) mediated ADCC, and (iii) reduced ocular disease in virus-infected mice. Herpes simplex virus 1 (HSV-1) causes cold sores and neonatal herpes and is a leading cause of blindness. Despite many trials, no HSV vaccine has been approved. Nectin-1 and HVEM are the two major cellular receptors for HSV. These receptors are expressed at different levels in various tissues, and the role of each receptor in HSV pathogenesis is not well understood. We derived human monoclonal antibodies from persons who received the HIV RV144 vaccine that contained the HVEM binding domain of HSV-1 gD fused to HIV gp120. These antibodies were able to specifically neutralize HSV-1 infection via HVEM. Furthermore, we showed for the first time that HVEM-specific HSV-1 neutralizing antibodies protect mice from HSV-1 eye disease, indicating the critical role of HVEM in HSV-1 ocular infection.
[Mh] Termos MeSH primário: Vacinas contra a AIDS/imunologia
Anticorpos Monoclonais/imunologia
Oftalmopatias/prevenção & controle
Proteína gp120 do Envelope de HIV/imunologia
Herpes Simples/prevenção & controle
Membro 14 de Receptores do Fator de Necrose Tumoral/imunologia
Simplexvirus/imunologia
Proteínas do Envelope Viral/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/administração & dosagem
Citotoxicidade Celular Dependente de Anticorpos/imunologia
Linhagem Celular
Oftalmopatias/virologia
Feminino
Proteína gp120 do Envelope de HIV/genética
Herpes Simples/imunologia
Herpes Simples/virologia
Seres Humanos
Células Matadoras Naturais/imunologia
Leucócitos Mononucleares/imunologia
Ativação Linfocitária/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Simplexvirus/genética
Proteínas do Envelope Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AIDS Vaccines); 0 (Antibodies, Monoclonal); 0 (HIV Envelope Protein gp120); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Viral Envelope Proteins); 0 (glycoprotein D, Human herpesvirus 1); 0 (gp120 protein, Human immunodeficiency virus 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE


  6 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28671524
[Au] Autor:Fujimoto Y; Tomioka Y; Ozaki K; Takeda K; Suyama H; Yamamoto S; Takakuwa H; Morimatsu M; Uede T; Ono E
[Ad] Endereço:1​Department of Biomedicine, Center of Biomedical Research, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan 2​Center of Biomedical Research, Research Center for Human Disease Modeling, Graduate School of Medical Sciences, Kyushu Univers
[Ti] Título:Comparison of the antiviral potential among soluble forms of herpes simplex virus type-2 glycoprotein D receptors, herpes virus entry mediator A, nectin-1 and nectin-2, in transgenic mice.
[So] Source:J Gen Virol;98(7):1815-1822, 2017 Jul.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Herpesvirus entry mediator A (HVEM), nectin-1 and nectin-2 are cellular receptors of glycoprotein D (gD) of herpes simplex virus type-2 (HSV-2). It has been shown that soluble forms of HSV gD receptors have the antiviral potential in cultured cells and transgenic mice. Here, to compare antiviral potential of soluble forms of HVEM, nectin-1 and nectin-2 against HSV-2 infections in vivo, transgenic mice expressing fusion proteins consisting of the entire ectodomain of HVEM, nectin-1 or nectin-2 and the Fc portion of human IgG (HVEMIg, nectin-1Ig and nectin-2Ig, respectively) were intraperitoneally infected with HSV-2. In the infection with 3 MLD50 (50 % mouse lethal dose), effective resistance was not observed in transgenic mice expressing nectin-2Ig. In a transgenic mouse line with high expression of nectin-1Ig, significant protection from the infection with 30 and 300 MLD50 was observed (survival rate of 100 and 71 %, respectively). On the other hand, transgenic mice expressing HVEMIg showed a complete resistance to the lethal infection even with 300 MLD50 (survival rate of 100 %). These results demonstrated that HVEMIg could exert effective antiviral activities against HSV-2 infections in vivo as compared with other soluble forms of HSV gD receptors.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/imunologia
Herpes Simples/imunologia
Herpesvirus Humano 2/metabolismo
Membro 14 de Receptores do Fator de Necrose Tumoral/imunologia
Receptores Virais/imunologia
Proteínas do Envelope Viral/metabolismo
[Mh] Termos MeSH secundário: Animais
Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/metabolismo
Herpes Simples/genética
Herpes Simples/metabolismo
Herpes Simples/virologia
Herpesvirus Humano 2/genética
Herpesvirus Humano 2/imunologia
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Nectinas
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
Receptores Virais/genética
Receptores Virais/metabolismo
Proteínas do Envelope Viral/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (NECTIN1 protein, human); 0 (Nectin1 protein, mouse); 0 (Nectins); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Receptors, Virus); 0 (Viral Envelope Proteins); 0 (glycoprotein D-herpes simplex virus type 2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000804


  7 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28594868
[Au] Autor:Spodzieja M; Lach S; Iwaszkiewicz J; Cesson V; Kalejta K; Olive D; Michielin O; Speiser DE; Zoete V; Derré L; Rodziewicz-Motowidlo S
[Ad] Endereço:University of Gdansk, Department of Chemistry, Gdansk, Poland.
[Ti] Título:Design of short peptides to block BTLA/HVEM interactions for promoting anticancer T-cell responses.
[So] Source:PLoS One;12(6):e0179201, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antibody based immune-checkpoint blockade therapy is a major breakthrough in oncology, leading to clinical benefit for cancer patients. Among the growing family of inhibitory receptors, the B and T lymphocyte attenuator (BTLA), which interacts with herpes virus entry mediator (HVEM), is a promising target for immunotherapy. Indeed, BTLA inhibits T-cell proliferation and cytokine production. The crystal structure of the BTLA/HVEM complex has shown that the HVEM(26-38) fragment is directly involved in protein binding. We designed and analyzed the capacity of several analogs of this fragment to block the ligation between BTLA and HVEM, using competitive ELISA and cellular assay. We found that the HVEM(23-39) peptide can block BTLA/HVEM ligation. However, the blocking ability was due to the Cys encompassed in this peptide and that even free cysteine targeted the BTLA protein and blocked its interaction with HVEM. These data highlight a Cys-related artefact in vitro, which should be taken in consideration for future development of BTLA/HVEM blocking compounds.
[Mh] Termos MeSH primário: Desenho de Drogas
Neoplasias/tratamento farmacológico
Neoplasias/imunologia
Peptídeos/síntese química
Peptídeos/uso terapêutico
Receptores Imunológicos/metabolismo
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Linhagem Celular
Cisteína/metabolismo
Seres Humanos
Neoplasias/patologia
Peptídeos/química
Peptídeos/farmacologia
Ligação Proteica/efeitos dos fármacos
Receptores Imunológicos/química
Membro 14 de Receptores do Fator de Necrose Tumoral/química
Linfócitos T/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BTLA protein, human); 0 (Peptides); 0 (Receptors, Immunologic); 0 (Receptors, Tumor Necrosis Factor, Member 14); K848JZ4886 (Cysteine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179201


  8 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28533310
[Au] Autor:Schmidt J; Ramis-Zaldivar JE; Nadeu F; Gonzalez-Farre B; Navarro A; Egan C; Montes-Mojarro IA; Marafioti T; Cabeçadas J; van der Walt J; Dojcinov S; Rosenwald A; Ott G; Bonzheim I; Fend F; Campo E; Jaffe ES; Salaverria I; Quintanilla-Martinez L
[Ad] Endereço:Institute of Pathology and Neuropathology, Eberhard Karls University of Tübingen and Comprehensive Cancer Center, Tübingen University Hospital, Tübingen, Germany.
[Ti] Título:Mutations of are frequent in pediatric-type follicular lymphoma and result in ERK pathway activation.
[So] Source:Blood;130(3):323-327, 2017 Jul 20.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pediatric-type follicular lymphoma (PTFL) is a B-cell lymphoma with distinctive clinicopathological features. Recently, recurrent genetic alterations of potential importance for its pathogenesis that disrupt pathways associated with the germinal center reaction ( , ), immune escape ( ), and anti-apoptosis ( ) have been described. In an attempt to shed more light onto the pathogenesis of PTFL, an integrative analysis of these mutations was undertaken in a large cohort of 43 cases previously characterized by targeted next-generation sequencing and copy number array. Mutations in were found in 49% (20/41) of the cases, second in frequency to alterations (22/41; 54%), and all together were present in 81% of the cases. Immunohistochemical analysis of the downstream target extracellular signal-regulated kinase demonstrated its phosphorylation in the evaluable cases and revealed a good correlation with the allelic frequency of the mutation. The p.K66R mutation was present in 15% (6/39) of the cases and was concomitant with mutations in 4 cases. This hot spot seems to be highly characteristic for PTFL. In conclusion, and mutations are the most frequent genetic alterations found in PTFL and occur independently in most cases, suggesting that both mutations might play an important role in PTFL lymphomagenesis.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Fatores Reguladores de Interferon/genética
Linfoma Folicular/genética
MAP Quinase Quinase 1/genética
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/genética
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Alelos
Carcinogênese/genética
Carcinogênese/metabolismo
Carcinogênese/patologia
Criança
Variações do Número de Cópias de DNA
Feminino
Perfilação da Expressão Gênica
Frequência do Gene
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Fatores Reguladores de Interferon/metabolismo
Linfoma Folicular/diagnóstico
Linfoma Folicular/metabolismo
Linfoma Folicular/patologia
MAP Quinase Quinase 1/metabolismo
Masculino
Análise em Microsséries
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Mutação
Fosforilação
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Regulatory Factors); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (TNFRSF14 protein, human); 0 (interferon regulatory factor-8); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.12.2 (MAP Kinase Kinase 1); EC 2.7.12.2 (MAP2K1 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-03-776278


  9 / 319 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28500993
[Au] Autor:Corbi-Botto CM; Sadaba SA; Zappa ME; Peral-García P; Díaz S
[Ad] Endereço:IGEVET - Instituto de Genética Veterinaria "Ing. Fernando Noel Dulout", (UNLP-CONICET LA PLATA), Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, CC 296. CP B1900AVW, La Plata, Argentina; Research fellows from Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET),
[Ti] Título:Nonsynonymous changes of equine lentivirus receptor-1 (ELR1) gene in amino acids involved in the interaction with equine infectious anemia virus (EIAV).
[So] Source:Res Vet Sci;112:185-191, 2017 Jun.
[Is] ISSN:1532-2661
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Equine lentivirus receptor-1 (ELR1) has been characterized as the specific functional receptor that mediates equine infectious anemia virus (EIAV) entrance to horse macrophages. This receptor is tumor necrosis factor receptor superfamily member 14 (TNFRSF14). The aim of this study was to investigate the occurrence of allelic variants in the coding sequence of equine TNFRSF14 gene by screening for single-nucleotide polymorphisms (SNPs) in different equine populations. Forty seven horse samples were randomly selected from a reservoir of EIAV-seropositive and seronegative samples collected from different outbreaks and regions of Argentina. DNA samples were scanned via PCR and direct sequencing of exon 3 and exon 5 of TNFRSF14 gene. A total of 21 SNPs were identified, of which 11 were located in coding sequences. Within exon 5, four SNPs caused nonsynonymous substitutions, while two other SNPs caused synonymous substitutions in crucial residues (Ser112 and Thr114) implicated in the interaction with EIAV. Despite some of exon 5 variants occurred exclusively in EIAV-positive or EIAV-negative horses, critical residues for the function of the mature protein were conserved, accounting for selective pressures in favor of preserving the specific function of TNFRSF members and the host immune response. To our knowledge, this is the first report of the existence of allelic variations involving some crucial amino acid residues in horse ELR1. Further, it could be an initial step to test the possible functional relevance and relationship of these variants with EIAV infection and disease progression as well as to develop preventive strategies.
[Mh] Termos MeSH primário: Anemia Infecciosa Equina/virologia
Regulação da Expressão Gênica/imunologia
Vírus da Anemia Infecciosa Equina
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Argentina/epidemiologia
Anemia Infecciosa Equina/epidemiologia
Cavalos/genética
Reação em Cadeia da Polimerase
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor, Member 14)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170514
[St] Status:MEDLINE


  10 / 319 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28423057
[Au] Autor:Petrovic B; Gianni T; Gatta V; Campadelli-Fiume G
[Ad] Endereço:Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, via S. Giacomo 12, Bologna, Italy.
[Ti] Título:Insertion of a ligand to HER2 in gB retargets HSV tropism and obviates the need for activation of the other entry glycoproteins.
[So] Source:PLoS Pathog;13(4):e1006352, 2017 Apr.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpes simplex virus (HSV) entry into the cells requires glycoproteins gD, gH/gL and gB, activated in a cascade fashion by conformational modifications induced by cognate receptors and intermolecular signaling. The receptors are nectin1 and HVEM (Herpes virus entry mediator) for gD, and αvß6 or αvß8 integrin for gH. In earlier work, insertion of a single chain antibody (scFv) to the cancer receptor HER2 (human epidermal growth factor receptor 2) in gD, or in gH, resulted in HSVs specifically retargeted to the HER2-positive cancer cells, hence in highly specific non-attenuated oncolytic agents. Here, the scFv to HER2 was inserted in gB (gBHER2). The insertion re-targeted the virus tropism to the HER2-positive cancer cells. This was unexpected since gB is known to be a fusogenic glycoprotein, not a tropism determinant. The gB-retargeted recombinant offered the possibility to investigate how HER2 mediated entry. In contrast to wt-gB, the activation of the chimeric gBHER2 did not require the activation of the gD and of gH/gL by their respective receptors. Furthermore, a soluble form of HER2 could replace the membrane-bound HER2 in mediating virus entry, hinting that HER2 acted by inducing conformational changes to the chimeric gB. This study shows that (i) gB can be modified and become the major determinant of HSV tropism; (ii) the chimeric gBHER2 bypasses the requirement for receptor-mediated activation of other essential entry glycoproteins.
[Mh] Termos MeSH primário: Glicoproteínas/metabolismo
Herpes Simples/virologia
Herpesvirus Humano 1/fisiologia
Receptor ErbB-2/metabolismo
Anticorpos de Cadeia Única/genética
[Mh] Termos MeSH secundário: Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/metabolismo
Glicoproteínas/genética
Herpes Simples/patologia
Herpesvirus Humano 1/genética
Herpesvirus Humano 1/patogenicidade
Seres Humanos
Integrinas/genética
Integrinas/metabolismo
Ligantes
Macrolídeos/farmacologia
Nectinas
Receptor ErbB-2/genética
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
Receptores Virais/genética
Receptores Virais/metabolismo
Proteínas Recombinantes de Fusão
Anticorpos de Cadeia Única/metabolismo
Tropismo Viral
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Glycoproteins); 0 (Integrins); 0 (Ligands); 0 (Macrolides); 0 (NECTIN1 protein, human); 0 (Nectins); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Receptors, Virus); 0 (Recombinant Fusion Proteins); 0 (Single-Chain Antibodies); 0 (integrin alphavbeta8); 116764-51-3 (bafilomycin A); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006352



página 1 de 32 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