Base de dados : MEDLINE
Pesquisa : D27.505.696.477.828 [Categoria DeCS]
Referências encontradas : 2852 [refinar]
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[PMID]:29227073
[Au] Autor:Uspenska KR; Gergalova GL; Lykhmus OY; Skok MV
[Ti] Título:The effect of amixin and agmatine on cytochrome C release from isolated mitochondria
[So] Source:Ukr Biochem J;88(1):5-10, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Mitochondrial nicotinic acetylcholine receptors (nAChRs) control permeability transition pore formation and cytochrome c release in the presence of apoptogenic factors. This study demonstrates that pharmacological agents amixin and agmatine affect mitochondrial nAChR functioning: they slightly suppress cytochrome c release from mouse brain and liver mitochondria stimulated with apoptogenic dose of Са2+ and prevent the effect of α7 nAChR agonist PNU282987. We conclude that mitochondria may be one of therapeutic targets of amixin and agmatine.
[Mh] Termos MeSH primário: Agmatina/farmacologia
Indutores de Interferon/farmacologia
Mitocôndrias/efeitos dos fármacos
Tilorona/farmacologia
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzamidas/antagonistas & inibidores
Benzamidas/farmacologia
Encéfalo/efeitos dos fármacos
Compostos Bicíclicos com Pontes/antagonistas & inibidores
Compostos Bicíclicos com Pontes/farmacologia
Cálcio/farmacologia
Fracionamento Celular
Citocromos c/antagonistas & inibidores
Citocromos c/secreção
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mitocôndrias/metabolismo
Agonistas Nicotínicos/farmacologia
Especificidade de Órgãos
Receptor Nicotínico de Acetilcolina alfa7/agonistas
Receptor Nicotínico de Acetilcolina alfa7/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (Bridged Bicyclo Compounds); 0 (Interferon Inducers); 0 (Nicotinic Agonists); 0 (PNU-282987); 0 (alpha7 Nicotinic Acetylcholine Receptor); 70J407ZL5Q (Agmatine); 9007-43-6 (Cytochromes c); O6W7VEW6KS (Tilorone); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.005


  2 / 2852 MEDLINE  
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[PMID]:28777803
[Au] Autor:Scholz T; Weigert A; Brüne B; Sadik CD; Böhm B; Burkhardt H
[Ad] Endereço:Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Project Group Translational Medicine & Pharmacology TMP, Goethe University, Frankfurt am Main, Germany.
[Ti] Título:GM-CSF in murine psoriasiform dermatitis: Redundant and pathogenic roles uncovered by antibody-induced neutralization and genetic deficiency.
[So] Source:PLoS One;12(8):e0182646, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a pleiotropic, Th17-derived cytokine thought to critically contribute to the pathogenesis of diverse autoimmune diseases, including rheumatoid arthritis and psoriasis. Treatment with monoclonal antibodies that block GM-CSF activity is associated with favorable therapeutic effects in patients with rheumatoid arthritis. We evaluated the role of GM-CSF as a potential target for therapeutic interference in psoriasis using a combined pharmacologic and genetic approach and the mouse model of imiquimod-induced psoriasiform dermatitis (IMQPD). Neutralization of murine GM-CSF by an anti-GM-CSF antibody ameliorated IMQPD. In contrast, genetic deficiency in GM-CSF did not alter the course of IMQPD, suggesting the existence of mechanisms compensating for chronic, but not acute, absence of GM-CSF. Further investigation uncovered an alternative pathogenic pathway for IMQPD in the absence of GM-CSF characterized by an expanded plasmacytoid dendritic cell population and release of IFNα and IL-22. This pathway was not activated in wild-type mice during short-term anti-GM-CSF treatment. Our investigations support the potential value of GM-CSF as a therapeutic target in psoriatic disease. The discovery of an alternative pathogenic pathway for psoriasiform dermatitis in the permanent absence of GM-CSF, however, suggests the need for monitoring during therapeutic use of long-term GM-CSF blockade.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Anticorpos Neutralizantes/farmacologia
Modelos Animais de Doenças
Fator Estimulador de Colônias de Granulócitos e Macrófagos/antagonistas & inibidores
Psoríase/tratamento farmacológico
[Mh] Termos MeSH secundário: Aminoquinolinas/toxicidade
Animais
Fator Estimulador de Colônias de Granulócitos e Macrófagos/imunologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Seres Humanos
Indutores de Interferon/toxicidade
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Psoríase/induzido quimicamente
Psoríase/imunologia
Psoríase/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Antibodies, Monoclonal); 0 (Antibodies, Neutralizing); 0 (Interferon Inducers); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182646


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[PMID]:28152141
[Au] Autor:Gao ML; Wu KC; Deng WL; Lei XL; Xiang L; Zhou GH; Feng CY; Cheng XW; Zhang CJ; Gu F; Wu RH; Jin ZB
[Ad] Endereço:Lab for Stem Cell & Retinal Regeneration, Institute of Stem Cell Research, Division of Ophthalmic Genetics, The Eye Hospital, Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Toll-Like Receptor 3 Activation Initiates Photoreceptor Cell Death In Vivo and In Vitro.
[So] Source:Invest Ophthalmol Vis Sci;58(2):801-811, 2017 Feb 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Accumulating evidence has demonstrated that excessive immunoreaction plays a prominent role in the pathogenesis of dry AMD. Toll-like receptor 3 (TLR3) can be activated by double-stranded (ds)RNA in retinal pigment epithelia and trigger an innate immunity-mediated inflammatory response. However, its role in photoreceptor cells, the effectors of AMD geographic atrophy, remains unclear. Methods: The expression of TLR3 was examined in mouse retina and in a murine photoreceptor cell line (661W). Retinal structure, function, and cell death in the polyinosine-polycytidylic acid (poly I:C)-treated retina were investigated by optical coherence tomography, electroretinography (ERG), and immunostaining. Cytokine and chemokine expression as well as cell death were measured in poly I:C-exposed 661W cells and explant retinas. By comparing the RNA sequencing (seq) data of 661W cells and murine retina, we comprehensively investigated the contribution of photoreceptor in poly I:C-induced retinal immune response. Results: Toll-like receptor 3 was highly expressed in the inner segment of the photoreceptor and in 661W cells. We found poly I:C induced significant retinal structural damages and impairment of ERG responses. Focal ERG demonstrated that injected and parainjected zones were functionally damaged by poly I:C. In addition, poly I:C acted on cultured photoreceptor cells directly and evoked an inflammatory response that exhibited similarities with the immune response in mouse retina. Moreover, TLR3 activation initiated cell death in murine photoreceptor cells in vivo and in vitro. Additionally, poly I:C initiated immune response in explant retinas. Conclusions: We deciphered the TLR3-mediated inflammatory response in photoreceptor cells. Our findings suggested TLR3-mediated inflammatory response in photoreceptor cells may play an important role in dry AMD, offering new insights of potential treatments targeting photoreceptor immunity.
[Mh] Termos MeSH primário: Morte Celular/fisiologia
Células Fotorreceptoras de Vertebrados/metabolismo
Retina/metabolismo
Receptor 3 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Morte Celular/efeitos dos fármacos
Linhagem Celular
Quimiocinas/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Eletrorretinografia
Indutores de Interferon/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Neuroglia/efeitos dos fármacos
Células Fotorreceptoras de Vertebrados/efeitos dos fármacos
Células Fotorreceptoras de Vertebrados/imunologia
Poli I-C/farmacologia
Retina/efeitos dos fármacos
Retina/fisiopatologia
Análise de Sequência de RNA
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Interferon Inducers); 0 (Toll-Like Receptor 3); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-20692


  4 / 2852 MEDLINE  
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[PMID]:28122258
[Au] Autor:da Silveira VT; Medeiros DC; Ropke J; Guidine PA; Rezende GH; Moraes MF; Mendes EM; Macedo D; Moreira FA; de Oliveira AC
[Ad] Endereço:Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Brazil.
[Ti] Título:Effects of early or late prenatal immune activation in mice on behavioral and neuroanatomical abnormalities relevant to schizophrenia in the adulthood.
[So] Source:Int J Dev Neurosci;58:1-8, 2017 May.
[Is] ISSN:1873-474X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Maternal immune activation (MIA) during pregnancy in rodents increases the risk of the offspring to develop schizophrenia-related behaviors, suggesting a relationship between the immune system and the brain development. Here we tested the hypothesis that MIA induced by the viral mimetic polyinosinic-polycytidylic acid (poly I:C) in early or late gestation of mice leads to behavioral and neuroanatomical disorders in the adulthood. On gestational days (GDs) 9 or 17 pregnant dams were treated with poly I:C or saline via intravenous route and the offspring behaviors were measured during adulthood. Considering the progressive structural neuroanatomical alterations in the brain of individuals with schizophrenia, we used magnetic resonance imaging (MRI) to perform brain morphometric analysis of the offspring aged one year. MIA on GD9 or GD17 led to increased basal locomotor activity, enhanced motor responses to ketamine, a psychotomimetic drug, and reduced time spent in the center of the arena, suggesting an increased anxiety-like behavior. In addition, MIA on GD17 reduced glucose preference in the offspring. None of the treatments altered the relative volume of the lateral ventricles. However, a decrease in brain volume, especially for posterior structures, was observed for one-year-old animals treated with poly I:C compared with control groups. Thus, activation of the maternal immune system at different GDs lead to neuroanatomical and behavioral alterations possibly related to the positive and negative symptoms of schizophrenia. These results provide insights on neuroimmunonological and neurodevelopmental aspects of certain psychopathologies, such as schizophrenia.
[Mh] Termos MeSH primário: Encéfalo/patologia
Transtornos Mentais/etiologia
Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
Esquizofrenia/complicações
Esquizofrenia/etiologia
Esquizofrenia/patologia
[Mh] Termos MeSH secundário: Fatores Etários
Análise de Variância
Animais
Animais Recém-Nascidos
Encéfalo/diagnóstico por imagem
Encéfalo/embriologia
Encéfalo/crescimento & desenvolvimento
Modelos Animais de Doenças
Embrião de Mamíferos
Feminino
Preferências Alimentares
Indutores de Interferon/toxicidade
Ketamina/toxicidade
Locomoção/fisiologia
Imagem por Ressonância Magnética
Camundongos
Camundongos Endogâmicos C57BL
Poli I-C/toxicidade
Gravidez
Esquizofrenia/diagnóstico por imagem
Sacarose/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Inducers); 57-50-1 (Sucrose); 690G0D6V8H (Ketamine); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE


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[PMID]:28115681
[Au] Autor:Herbert C; Do K; Chiu V; Garthwaite L; Chen Y; Young PM; Traini D; Kumar RK
[Ad] Endereço:Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia.
[Ti] Título:Allergic environment enhances airway epithelial pro-inflammatory responses to rhinovirus infection.
[So] Source:Clin Sci (Lond);131(6):499-509, 2017 Mar 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Airway epithelial cells (AEC) exhibit a pro-inflammatory phenotype in patients with allergic asthma. We examined the effect of an allergic cytokine environment on the response of AEC to rhinovirus (RV), the most common trigger of acute exacerbations of asthma. Calu-3 cells, a well-differentiated human AEC line, were cultured with or without the T-helper type 2 cytokines interleukin (IL)-4 and IL-13, then stimulated with a toll-like receptor (TLR) 3 agonist (poly I:C, dsRNA) or a TLR7 agonist (imiquimod), or infected with RV 16. Expression of pro-inflammatory and antiviral mediators, and of viral pattern-recognition molecules, was assessed using nCounter assays, quantitative real-time PCR (qRT-PCR) and protein immunoassays. Both dsRNA and imiquimod stimulated expression of mRNA for whereas expression of several chemokines and antiviral response genes was induced only by dsRNA. Conversely, expression of other cytokines and growth factors was induced only by imiquimod. RV infection not only stimulated expression of the inflammation-related genes induced by dsRNA, but also of complement factor B and the novel pro-inflammatory cytokine IL-32. In the T helper type 2 (Th2) cytokine environment, several mediators exhibited significantly enhanced expression, whereas expression of interferons was either unchanged or enhanced. The allergic environment also increased expression of pattern-recognition receptors and of intercellular adhesion molecule 1, the cell surface receptor for RV. We conclude that Th2 cytokines promote increased production of pro-inflammatory mediators by AEC following infection with RV. Increased viral entry or enhanced signalling via pattern-recognition receptors could also contribute to the exaggerated inflammatory response to RV observed in allergic asthmatics.
[Mh] Termos MeSH primário: Mediadores da Inflamação/metabolismo
Infecções por Picornaviridae/metabolismo
Mucosa Respiratória/virologia
Rhinovirus
[Mh] Termos MeSH secundário: Aminoquinolinas/farmacologia
Asma/imunologia
Asma/metabolismo
Asma/virologia
Células Cultivadas
Citocinas/biossíntese
Citocinas/genética
Células Epiteliais/metabolismo
Células Epiteliais/virologia
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/genética
Seres Humanos
Indutores de Interferon/farmacologia
Infecções por Picornaviridae/genética
Infecções por Picornaviridae/imunologia
Poli I-C/farmacologia
RNA de Cadeia Dupla/genética
RNA Mensageiro/genética
Mucosa Respiratória/metabolismo
Células Th2/imunologia
Receptor 3 Toll-Like/agonistas
Receptor 7 Toll-Like/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Cytokines); 0 (Inflammation Mediators); 0 (Interferon Inducers); 0 (RNA, Double-Stranded); 0 (RNA, Messenger); 0 (TLR3 protein, human); 0 (TLR7 protein, human); 0 (Toll-Like Receptor 3); 0 (Toll-Like Receptor 7); O84C90HH2L (Poly I-C); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1042/CS20160939


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[PMID]:28110790
[Au] Autor:Zhang X; Wang J; Mao Y; Xi J; Yu Y; Liu W
[Ad] Endereço:State Key Laboratory of Agrobiotechnology, Department of Biochemistry and Molecular Biology, College of Biological Sciences, China Agricultural University, Beijing 100193, PR China.
[Ti] Título:Induction and suppression of type I interferon responses by mink enteritis virus in CRFK cells.
[So] Source:Vet Microbiol;199:8-14, 2017 Feb.
[Is] ISSN:1873-2542
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mink enteritis virus (MEV) is one of the most important viral pathogens causing serious disease in mink. Type I interferon (IFN) plays a critical role in antiviral innate immunity and, for successful infection, many viruses have evolved evasive strategies against it. Here, we show that MEV infection does not evoke IFN or interferon-stimulated genes (ISGs) responses in feline kidney (CRFK) cells, and that MEV suppresses IFN production in both poly I:C-stimulated and untreated cells. In CRFK cells pre-exposure to IFN, show that infection with, and replication of, MEV remain unaffected. This inhibition appears to be mediated by the MEV nonstructural protein (NS1) with its ORI-binding domain playing a major role.
[Mh] Termos MeSH primário: Panleucopenia Felina/imunologia
Interferon Tipo I/imunologia
Vírus da Enterite do Vison/fisiologia
[Mh] Termos MeSH secundário: Animais
Gatos
Linhagem Celular
Regulação da Expressão Gênica/efeitos dos fármacos
Indutores de Interferon/farmacologia
Poli I-C/farmacologia
Proteínas não Estruturais Virais/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Inducers); 0 (Interferon Type I); 0 (Viral Nonstructural Proteins); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE


  7 / 2852 MEDLINE  
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[PMID]:28109979
[Au] Autor:Shirai K; Shimada T; Yoshida H; Hayakari R; Matsumiya T; Tanji K; Murakami M; Tanaka H; Imaizumi T
[Ad] Endereço:Department of Vascular Biology, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan.
[Ti] Título:Interferon (IFN)-induced protein 35 (IFI35) negatively regulates IFN-ß-phosphorylated STAT1-RIG-I-CXCL10/CCL5 axis in U373MG astrocytoma cells treated with polyinosinic-polycytidylic acid.
[So] Source:Brain Res;1658:60-67, 2017 Mar 01.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Interferon (IFN)-stimulated genes (ISGs) exert multiple functions in immune system. IFN-induced protein 35 (IFI35) is a member of ISGs, and has been suggested to regulate innate immune reaction. However, the physiological functions and pathological roles of IFI35 in the central nervous system are not characterized well. In the present study, we found that the expression of IFI35 was induced by a Toll-like receptor 3 (TLR3) ligand polyinosinic-polycytidylic acid (poly IC) in U373MG human astrocytoma cells. Knockdown of IFI35 using RNA interference resulted in increased expression of IFN-ß, phosphorylated STAT1 (P-STAT1), retinoic acid-inducible gene-I (RIG-I), CXCL10 and CCL5 induced by poly IC. Poly IC-induced expression of CXCL10 and CCL5 was decreased by knockdown of RIG-I. These results suggest that IFI35 may negatively regulate the TLR3-IFN-ß-P-STAT1-RIG-I-CXCL10/CCL5 axis in U373MG cells, and IFI35 may play a role at least partially in the regulation of innate immune reactions in astrocytes.
[Mh] Termos MeSH primário: Astrócitos/efeitos dos fármacos
Astrócitos/imunologia
Indutores de Interferon/farmacologia
Interferon beta/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Poli I-C/farmacologia
[Mh] Termos MeSH secundário: Astrocitoma/imunologia
Linhagem Celular Tumoral
Quimiocina CCL5/metabolismo
Quimiocina CXCL10/metabolismo
Citoplasma/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Fosforilação/efeitos dos fármacos
Fosforilação/fisiologia
RNA Mensageiro/metabolismo
Receptores do Ácido Retinoico/genética
Receptores do Ácido Retinoico/metabolismo
Fator de Transcrição STAT1/metabolismo
Receptor 3 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL5 protein, human); 0 (CXCL10 protein, human); 0 (Chemokine CCL5); 0 (Chemokine CXCL10); 0 (IFI35 protein, human); 0 (Interferon Inducers); 0 (Intracellular Signaling Peptides and Proteins); 0 (RARRES3 protein, human); 0 (RNA, Messenger); 0 (Receptors, Retinoic Acid); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (TLR3 protein, human); 0 (Toll-Like Receptor 3); 77238-31-4 (Interferon-beta); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170123
[St] Status:MEDLINE


  8 / 2852 MEDLINE  
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[PMID]:28052019
[Au] Autor:Wu J; Li S; Yang Y; Zhu S; Zhang M; Qiao Y; Liu YJ; Chen J
[Ad] Endereço:Institute of Translational Medicine, The First Hospital, Jilin University, Changchun, 130061, China.
[Ti] Título:TLR-activated plasmacytoid dendritic cells inhibit breast cancer cell growth in vitro and in vivo.
[So] Source:Oncotarget;8(7):11708-11718, 2017 Feb 14.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasmacytoid dendritic cells (pDCs) are a unique subset of naturally occurring dendritic cells, which triggers the production of large amounts of type I interferons (IFNs) after viral infections through Toll-like receptor (TLR) 7 and TLR9. Recent studies have demonstrated that the activation of pDCs kills melanoma cells. However, the role of activated pDCs in breast cancer remains to be determined. In the present study, we generated mouse models of breast cancer and demonstrated that activated pDCs can directly kill breast tumor cells through TRAIL and Granzyme B. Furthermore, we established that pDCs initiate the sequential activation of NK cells and CD8+ T cells, and ultimately inhibit breast tumor growth. Understanding the role of activated pDCs in breast cancer may help to develop new strategies for manipulating the function of pDCs and induce anti-tumor immunity in breast cancer.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Células Dendríticas/transplante
Imunoterapia Adotiva/métodos
Neoplasias Mamárias Experimentais/imunologia
Neoplasias Mamárias Experimentais/terapia
Glicoproteínas de Membrana/imunologia
Receptor 7 Toll-Like/imunologia
[Mh] Termos MeSH secundário: Aminoquinolinas/farmacologia
Animais
Células Dendríticas/patologia
Modelos Animais de Doenças
Feminino
Granzimas/imunologia
Indutores de Interferon/farmacologia
Neoplasias Mamárias Experimentais/patologia
Camundongos
Camundongos Endogâmicos BALB C
Ligante Indutor de Apoptose Relacionado a TNF/imunologia
Receptor Toll-Like 9/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Interferon Inducers); 0 (Membrane Glycoproteins); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (Tlr7 protein, mouse); 0 (Tlr9 protein, mouse); 0 (Tnfsf10 protein, mouse); 0 (Toll-Like Receptor 7); 0 (Toll-Like Receptor 9); EC 3.4.21.- (Granzymes); EC 3.4.21.- (Gzmb protein, mouse); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170105
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14315


  9 / 2852 MEDLINE  
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[PMID]:27993525
[Au] Autor:Zevallos VF; Raker V; Tenzer S; Jimenez-Calvente C; Ashfaq-Khan M; Rüssel N; Pickert G; Schild H; Steinbrink K; Schuppan D
[Ad] Endereço:Institute of Translational Immunology, University Medical Center, Johannes Gutenberg University, Mainz, Germany; Research Center for Immunotherapy, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
[Ti] Título:Nutritional Wheat Amylase-Trypsin Inhibitors Promote Intestinal Inflammation via Activation of Myeloid Cells.
[So] Source:Gastroenterology;152(5):1100-1113.e12, 2017 Apr.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Wheat amylase-trypsin inhibitors (ATIs) are nutritional activators of innate immunity, via activation of the toll-like receptor 4 (TLR4) on myeloid cells. We aimed to characterize the biologic activity of ATIs in various foods and their effect on intestinal inflammation. METHODS: We selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat, rye, barley, quinoa, amaranth, soya, lentils, and rice) or processed (such as pizza, pasta, bread, and biscuits). ATIs were extracted and their biological activities determined in TLR4-responsive mouse and human cell lines. Effects of oral ATIs on intestinal inflammation were determined in healthy C57BL/6 mice on a gluten-free or ATI-free diet and in mice given low-level polyinosinic:polycytidylic acid or dextran sodium sulfate to induce colitis. Parameters of innate and adaptive immune activation were determined in duodenum, ileum, colon, and mesenteric lymph nodes. RESULTS: Modern gluten-containing staples had levels of TLR4-activating ATIs that were as much as 100-fold higher than in most gluten-free foods. Processed or baked foods retained ATI bioactivity. Most older wheat variants (such as Emmer or Einkorn) had lower bioactivity than modern (hexaploid) wheat. ATI species CM3 and 0.19 were the most prevalent activators of TLR4 in modern wheat and were highly resistant to intestinal proteolysis. Their ingestion induced modest intestinal myeloid cell infiltration and activation, and release of inflammatory mediators-mostly in the colon, then in the ileum, and then in the duodenum. Dendritic cells became prominently activated in mesenteric lymph nodes. Concentrations of ATIs found in a normal daily gluten-containing diet increased low-level intestinal inflammation. CONCLUSIONS: Gluten-containing cereals have by far the highest concentrations of ATIs that activate TLR4. Orally ingested ATIs are largely resistant to proteases and heat, and increase intestinal inflammation by activating gut and mesenteric lymph node myeloid cells.
[Mh] Termos MeSH primário: Amilases/antagonistas & inibidores
Doença Celíaca/imunologia
Colite/imunologia
Glutens/imunologia
Intestinos/imunologia
Células Mieloides/imunologia
Receptor 4 Toll-Like/imunologia
Inibidores da Tripsina/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Linhagem Celular
Colite/induzido quimicamente
Colo/imunologia
Sulfato de Dextrana/toxicidade
Dieta Livre de Glúten
Duodeno/imunologia
Seres Humanos
Íleo/imunologia
Imunidade Inata/imunologia
Inflamação
Indutores de Interferon/toxicidade
Linfonodos/imunologia
Mesentério
Camundongos
Camundongos Endogâmicos C57BL
Proteínas de Plantas/imunologia
Poli I-C/toxicidade
Triticum/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Inducers); 0 (Plant Proteins); 0 (Toll-Like Receptor 4); 0 (Trypsin Inhibitors); 8002-80-0 (Glutens); 9042-14-2 (Dextran Sulfate); EC 3.2.1.- (Amylases); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


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[PMID]:27895126
[Au] Autor:Kang I; Harten IA; Chang MY; Braun KR; Sheih A; Nivison MP; Johnson PY; Workman G; Kaber G; Evanko SP; Chan CK; Merrilees MJ; Ziegler SF; Kinsella MG; Frevert CW; Wight TN
[Ad] Endereço:From the Matrix Biology Program and.
[Ti] Título:Versican Deficiency Significantly Reduces Lung Inflammatory Response Induced by Polyinosine-Polycytidylic Acid Stimulation.
[So] Source:J Biol Chem;292(1):51-63, 2017 Jan 06.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Viral infection is an exacerbating factor contributing to chronic airway diseases, such as asthma, via mechanisms that are still unclear. Polyinosine-polycytidylic acid (poly(I:C)), a Toll-like receptor 3 (TLR3) agonist used as a mimetic to study viral infection, has been shown to elicit inflammatory responses in lungs and to exacerbate pulmonary allergic reactions in animal models. Previously, we have shown that poly(I:C) stimulates lung fibroblasts to accumulate an extracellular matrix (ECM), enriched in hyaluronan (HA) and its binding partner versican, which promotes monocyte adhesion. In the current study, we aimed to determine the in vivo role of versican in mediating inflammatory responses in poly(I:C)-induced lung inflammation using a tamoxifen-inducible versican-deficient mouse model (Vcan mice). In C57Bl/6 mice, poly(I:C) instillation significantly increased accumulation of versican and HA, especially in the perivascular and peribronchial regions, which were enriched in infiltrating leukocytes. In contrast, versican-deficient (Vcan ) lungs did not exhibit increases in versican or HA in these regions and had strikingly reduced numbers of leukocytes in the bronchoalveolar lavage fluid and lower expression of inflammatory chemokines and cytokines. Poly(I:C) stimulation of lung fibroblasts isolated from control mice generated HA-enriched cable structures in the ECM, providing a substrate for monocytic cells in vitro, whereas lung fibroblasts from Vcan mice did not. Moreover, increases in proinflammatory cytokine expression were also greatly attenuated in the Vcan lung fibroblasts. These findings provide strong evidence that versican is a critical inflammatory mediator during poly(I:C)-induced acute lung injury and, in association with HA, generates an ECM that promotes leukocyte infiltration and adhesion.
[Mh] Termos MeSH primário: Quimiocinas/metabolismo
Citocinas/metabolismo
Indutores de Interferon/toxicidade
Pneumonia/prevenção & controle
Poli I-C/toxicidade
Versicanas/fisiologia
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar/química
Células Cultivadas
Feminino
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monócitos/citologia
Monócitos/efeitos dos fármacos
Monócitos/metabolismo
Pneumonia/induzido quimicamente
Pneumonia/metabolismo
Pneumonia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokines); 0 (Cspg2 protein, mouse); 0 (Cytokines); 0 (Interferon Inducers); 126968-45-4 (Versicans); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.753186



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