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  1 / 42504 MEDLINE  
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[PMID]:29447181
[Au] Autor:Chen KYH; Messina N; Germano S; Bonnici R; Freyne B; Cheung M; Goldsmith G; Kollmann TR; Levin M; Burgner D; Curtis N
[Ad] Endereço:Murdoch Children's Research Institute, The Royal Children's Hospital, Melbourne, Vic, Australia.
[Ti] Título:Innate immune responses following Kawasaki disease and toxic shock syndrome.
[So] Source:PLoS One;13(2):e0191830, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pathogenesis of Kawasaki disease (KD) remains unknown and there is accumulating evidence for the importance of the innate immune system in initiating and mediating the host inflammatory response. We compared innate immune responses in KD and toxic shock syndrome (TSS) participants more than two years after their acute illness with control participants to investigate differences in their immune phenotype. Toxic shock syndrome shares many clinical features with KD; by including both disease groups we endeavoured to explore changes in innate immune responses following acute inflammatory illnesses more broadly. We measured the in vitro production of interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, IL-1 receptor antagonist (IL-1ra), and IL-10 following whole blood stimulation with toll-like receptor and inflammasome ligands in 52 KD, 20 TSS, and 53 control participants in a case-control study. Analyses were adjusted for age, sex, and unstimulated cytokine concentrations. Compared to controls, KD participants have reduced IL-1ra production in response to stimulation with double stranded RNA (geometric mean ratio (GMR) 0.37, 95% CI 0.15, 0.89, p = 0.03) and increased IL-6 production in response to incubation with Lyovec™ (GMR 5.48, 95% CI 1.77, 16.98, p = 0.004). Compared to controls, TSS participants have increased IFN-γ production in response to peptidoglycan (GMR 4.07, 95% CI 1.82, 9.11, p = 0.001), increased IL-1ß production to lipopolysaccharide (GMR 1.64, 95% CI 1.13, 2.38, p = 0.01) and peptidoglycan (GMR 1.61, 95% CI 1.11, 2.33, p = 0.01), and increased IL-6 production to peptidoglycan (GMR 1.45, 95% CI 1.10, 1.92, p = 0.01). Years following the acute illness, individuals with previous KD or TSS exhibit a pro-inflammatory innate immune phenotype suggesting a possible underlying immunological susceptibility or innate immune memory.
[Mh] Termos MeSH primário: Imunidade Inata
Síndrome de Linfonodos Mucocutâneos/imunologia
Choque Séptico/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Criança
Feminino
Seres Humanos
Inflamassomos/metabolismo
Masculino
Receptores Toll-Like/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191830


  2 / 42504 MEDLINE  
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[PMID]:29380441
[Au] Autor:Waugh CA; Arukwe A; Jaspers VLB
[Ad] Endereço:Environmental Toxicology, Department of Biology, Faculty of Natural Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
[Ti] Título:Deregulation of microRNA-155 and its transcription factor NF-kB by polychlorinated biphenyls during viral infections.
[So] Source:APMIS;126(3):234-240, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Polychlorinated biphenyls (PCBs), and similar environmental contaminants, have been linked to virus outbreaks and increased viral induced mortality since the 1970s. Yet the mechanisms behind this increased susceptibility remain elusive. It has recently been illustrated that the innate immune viral detection system is tightly regulated by small non-coding RNAs, including microRNAs (miRNAs). For virus infections miRNA-155 expression is an important host response against infection, and deregulation of this miRNA is closely associated with adverse outcomes. Thus, we designed a targeted in vitro study using primary chicken fibroblasts, first exposed to a mixture of PCBs (Arochlor-1250) before being stimulated with a synthetic RNA virus (poly I:C), to determine if PCBs have the potential to deregulate miRNA-155. In this paper, we provide the first data for the deregulation of miRNA-155 when a host is exposed to a mixture of PCBs before a virus infection. Thus, we provide important evidence that PCBs can be involved in the deregulation of important miRNA pathways involved in the immune system; thereby demonstrating novel insights into the mechanism of PCB toxicity on the immune system.
[Mh] Termos MeSH primário: Imunidade Inata/genética
MicroRNAs/genética
NF-kappa B/genética
Poli I-C/farmacologia
Bifenilos Policlorados/química
Vírus/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Embrião de Galinha
Galinhas/genética
Galinhas/imunologia
Regulação da Expressão Gênica/imunologia
Seres Humanos
Viroses/genética
Viroses/imunologia
Viroses/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); DFC2HB4I0K (Polychlorinated Biphenyls); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12811


  3 / 42504 MEDLINE  
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[PMID]:29377929
[Au] Autor:Allard D; Charlebois R; Gilbert L; Stagg J; Chrobak P
[Ad] Endereço:Centre de Recherche du Centre Hospitalier l'Université de Montréal (CRCHUM), Faculté de Pharmacie de l'Université de Montréal et Institut du Cancer de Montréal, Montréal, Quebec, Canada.
[Ti] Título:CD73-A2a adenosine receptor axis promotes innate B cell antibody responses to pneumococcal polysaccharide vaccination.
[So] Source:PLoS One;13(1):e0191973, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many individuals at risk of streptococcal infection respond poorly to the pneumococcal polysaccharide vaccine Pneumovax 23. Identification of actionable pathways able to enhance Pneumovax responsiveness is highly relevant. We investigated the contribution of the extracellular adenosine pathway regulated by the ecto-nucleotidase CD73 in Pneumovax-induced antibody responses. Using gene-targeted mice, we demonstrated that CD73-or A2a adenosine receptor deficiency significantly delayed isotype switching. Nevertheless, CD73- or A2aR- deficient adult mice ultimately produced antigen-specific IgG3 and controlled Streptococcus pneumoniae infection as efficiently as wild type (WT) mice. Compared to adults, young WT mice failed to control S. pneumoniae infection after vaccination and this was associated with lower levels of CD73 on innate B cells. We hypothesized that pharmacological activation of A2a receptor may improve Pneumovax 23 immunization in young WT mice. Remarkably, administration of the A2a adenosine receptor agonist CGS 21680 significantly increased IgG3 responses and significantly enhanced survival after S. pneumoniae challenge. Our study thus suggests that pharmacological activation of the A2a adenosine receptor could improve the efficacy of Pneumovax 23 vaccination in individuals at risk of streptococcal infection.
[Mh] Termos MeSH primário: 5´-Nucleotidase/metabolismo
Linfócitos B/imunologia
Imunidade Inata
Vacinas Pneumocócicas/imunologia
Receptor A2A de Adenosina/metabolismo
[Mh] Termos MeSH secundário: 5'-Nucleotidase/genética
Animais
Ensaio de Imunoadsorção Enzimática
Imunofluorescência
Imunoglobulina G/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptor A2A de Adenosina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoglobulin G); 0 (Pneumococcal Vaccines); 0 (Receptor, Adenosine A2A); EC 3.1.3.5 (5'-Nucleotidase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191973


  4 / 42504 MEDLINE  
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[PMID]:29337391
[Au] Autor:Ishii T; Niikura Y; Kurata K; Muroi M; Tanamoto K; Nagase T; Sakaguchi M; Yamashita N
[Ad] Endereço:Department of Pharmacotherapy, Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan.
[Ti] Título:Time-dependent distinct roles of Toll-like receptor 4 in a house dust mite-induced asthma mouse model.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:House dust mites (HDMs) are a common source of allergens that trigger both allergen-specific and innate immune responses in humans. Here, we examined the effect of allergen concentration and the involvement of Toll-like receptor 4 (TLR4) in the process of sensitization to house dust mite allergens in an HDM extract-induced asthma mouse model. Intranasal administration of HDM extract induced an immunoglobulin E response and eosinophilic inflammation in a dose-dependent manner from 2.5 to 30 µg/dose. In TLR4-knockout mice, the infiltration of eosinophils and neutrophils into the lung was decreased compared with that in wild-type mice in the early phase of inflammation (total of three doses). However, in the late phase of inflammation (total of seven doses), eosinophil infiltration was significantly greater in TLR4-knockout mice than in wild-type mice. This suggests that the roles of TLR4 signaling are different between the early phase and the later phase of HDM allergen-induced inflammation. Thus, innate immune response through TLR4 regulated the response to HDM allergens, and the regulation was altered during the phase of inflammation.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Antígenos de Dermatophagoides/imunologia
Asma/imunologia
Imunidade Inata/imunologia
Pyroglyphidae/imunologia
Receptor 4 Toll-Like/imunologia
[Mh] Termos MeSH secundário: Resistência das Vias Respiratórias/imunologia
Animais
Líquido da Lavagem Broncoalveolar/citologia
Modelos Animais de Doenças
Eosinófilos/patologia
Feminino
Imunização
Imunoglobulina E/imunologia
Inflamação/imunologia
Pulmão/citologia
Pulmão/imunologia
Pulmão/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infiltração de Neutrófilos/imunologia
Neutrófilos/patologia
Transdução de Sinais/imunologia
Receptor 4 Toll-Like/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Antigens, Dermatophagoides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12641


  5 / 42504 MEDLINE  
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[PMID]:29268133
[Au] Autor:Zhu G; Xu Y; Cen X; Nandakumar KS; Liu S; Cheng K
[Ad] Endereço:Guangdong Provincial Key Laboratory of New Drug Screening and Guangzhou Key Laboratory of Drug Research for Emerging Virus Prevention and Treatment, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
[Ti] Título:Targeting pattern-recognition receptors to discover new small molecule immune modulators.
[So] Source:Eur J Med Chem;144:82-92, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Pattern recognition receptors (PRRs) are key immune receptors of the innate immune system, which recognize the conserved pathogen-associated molecular patterns (PAMPs) of the invading pathogens. Compared to the adaptive immune receptors, PRRs have three distinguishing features, viz., universal expression, fast response and recognizing many kinds of microbes. Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), C-type lectin receptors (CLRs) and NOD-like receptors (NLRs) recognize viral nucleic acid/bacterial fragments and trigger anti-microbial innate immune responses. Upon recognition of their ligand species, PRRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in the activation of nuclear factor-κB (NF-κB), mitogen-activated protein (MAP) kinases and interferon regulatory factors (IRFs) that control the transcription of genes encoding pro-inflammatory factors including type I interferon and other inflammatory cytokines, which are critical for eliminating the potential threat to the host. Here, we summarize the effects of small molecule regulators acting on signaling pathways initiated by TLR, RLR and NLR as well as their influence on innate and adaptive immune responses leading to therapy.
[Mh] Termos MeSH primário: Imunidade Adaptativa/efeitos dos fármacos
Imunidade Inata/efeitos dos fármacos
Fatores Imunológicos/química
Fatores Imunológicos/farmacologia
Receptores de Reconhecimento de Padrão/imunologia
[Mh] Termos MeSH secundário: Animais
Descoberta de Drogas
Seres Humanos
Inflamação/tratamento farmacológico
Inflamação/imunologia
Terapia de Alvo Molecular
Bibliotecas de Moléculas Pequenas/química
Bibliotecas de Moléculas Pequenas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Immunologic Factors); 0 (Receptors, Pattern Recognition); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  6 / 42504 MEDLINE  
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[PMID]:28456536
[Au] Autor:More Bayona JA; Karuppannan AK; Barreda DR
[Ad] Endereço:Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2P5, Canada.
[Ti] Título:Contribution of leukocytes to the induction and resolution of the acute inflammatory response in chickens.
[So] Source:Dev Comp Immunol;74:167-177, 2017 Sep.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A successful immune response against invading pathogens relies on the efficient activation of host defense mechanisms and a timely return to immune homeostasis. Despite their importance, these mechanisms remain ill-defined in most animal groups. This study focuses on the acute inflammatory response of chickens, important both as an avian model with a unique position in evolution as well as an increasingly notable target of infectious zoonotic diseases. We took advantage of an in vivo self-resolving intra-abdominal challenge model to provide an integrative view of leukocyte responses during the induction and resolution phases of acute inflammation. Our results showed rapid leukocyte infiltration into the abdominal cavity post zymosan challenge (significant increase as early as 4 h), which was dominated by heterophils. Peak leukocyte infiltration and ROS production reached maximum levels at 12 h post challenge, which was significantly earlier than comparative studies in teleost fish and mice. Both heterophils and monocyte/macrophages contributed to ROS production. Local leukocyte infiltration was preceded by an increase in peripheral leukocytes and a drop in the number of bone marrow leukocytes. The proportion of apoptotic leukocytes increased following peak of acute inflammation, rising to significant levels within the abdominal cavity by 48 h, consistent with other indicators for the resolution of inflammation. Importantly, comparison of chicken phagocytic responses with those previously shown in agnathan, teleost and murine models suggested a progressive evolutionary shift towards an increased sensitivity to pro-inflammatory pathogen-derived particles and decreased sensitivity towards homeostatic stimuli. Thus, while significant conservation can be noted across the immune systems of endotherms, this study highlights additional unique features that govern the induction and resolution of acute inflammation in the avian system, which may be relevant to disease susceptibility and performance.
[Mh] Termos MeSH primário: Doenças das Aves/imunologia
Galinhas/imunologia
Inflamação/imunologia
Leucócitos/imunologia
Peritônio/fisiologia
Zoonoses/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Apoptose
Evolução Biológica
Movimento Celular
Proliferação Celular
Peixes
Seres Humanos
Imunidade Inata
Camundongos
Fagocitose
Fisiologia Comparada
Espécies Reativas de Oxigênio/metabolismo
Zimosan/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 9010-72-4 (Zymosan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  7 / 42504 MEDLINE  
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[PMID]:28452704
[Au] Autor:Yan CH; Hahn S; McMahon D; Bonislawski D; Kennedy DW; Adappa ND; Palmer JN; Jiang P; Lee RJ; Cohen NA
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Division of Rhinology, University of Pennsylvania, Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
[Ti] Título:Nitric oxide production is stimulated by bitter taste receptors ubiquitously expressed in the sinonasal cavity.
[So] Source:Am J Rhinol Allergy;31(2):85-92, 2017 Mar 01.
[Is] ISSN:1945-8932
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bitter taste receptors (T2R) have recently been demonstrated to contribute to sinonasal innate immunity. One T2R, T2R38, regulates mucosal defense against gram-negative organisms through nitric oxide (NO) production, which enhances mucociliary clearance and directly kills bacteria. To determine whether additional T2Rs contribute to this innate defense, we evaluated two other sinonasal T2Rs (T2R4 and T2R16) for regulation of NO production and expression within the human sinonasal cavity. METHODS: Primary human sinonasal cultures were stimulated with ligands specific to T2R4 and T2R16, colchicine and D-salicin, respectively. Cellular NO production was measured by intracellular 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate fluorescence. For T2R expression mapping, sinonasal tissue was obtained from patients who underwent sinus surgery of the middle turbinate, maxillary sinus, ethmoid sinus, or sphenoid sinus. The expression of T2R4, T2R16, and T2R38 was evaluated by using immunofluorescence with validated antibodies. RESULTS: Similar to T2R38, T2R4 and T2R16 trigger NO production in a dose-dependent manner by using the canonical taste signaling pathway in response to stimulation with their respective ligands. All three receptors were expressed in the cilia of human epithelial cells of all regions in the sinonasal cavity. CONCLUSION: These three T2Rs signaled through the same NO-mediated antimicrobial pathway and were ubiquitously expressed in the sinonasal epithelium. Additional T2Rs besides T2R38 may play a role in sinonasal immune defense. Mapping of T2R expression demonstrated the potential widespread role of T2Rs in sinonasal defense, whereas the genetics of these T2Rs may contribute to our understanding of specific endotypes of chronic rhinosinusitis and develop into novel therapeutic targets.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Mucosa Nasal/imunologia
Seios Paranasais/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Rinite/imunologia
Sinusite/imunologia
Paladar
[Mh] Termos MeSH secundário: Bacteriólise
Células Cultivadas
Doença Crônica
Seres Humanos
Imunidade Inata
Depuração Mucociliar
Mucosa Nasal/microbiologia
Óxido Nítrico/metabolismo
Cultura Primária de Células
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, G-Protein-Coupled); 0 (taste receptors, type 2); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2500/ajra.2017.31.4424


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[PMID]:28465096
[Au] Autor:Nicoli F; Appay V
[Ad] Endereço:Sorbonne Universités, UPMC Univ Paris 06, DHU FAST, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), F-75013 Paris, France; INSERM, U1135, CIMI-Paris, F-75013 Paris, France. Electronic address: nclfnc1@unife.it.
[Ti] Título:Immunological considerations regarding parental concerns on pediatric immunizations.
[So] Source:Vaccine;35(23):3012-3019, 2017 05 25.
[Is] ISSN:1873-2518
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Despite the fundamental role of vaccines in the decline of infant mortality, parents may decide to decline vaccination for their own children. Many factors may influence this decision, such as the belief that the infant immune system is weakened by vaccines, and concerns have been raised about the number of vaccines and the early age at which they are administered. Studies focused on the infant immune system and its reaction to immunizations, summarized in this review, show that vaccines can overcome those suboptimal features of infant immune system that render them more at risk of infections and of their severe manifestations. In addition, many vaccines have been shown to improve heterologous innate and adaptive immunity resulting in lower mortality rates for fully vaccinated children. Thus, multiple vaccinations are necessary and not dangerous, as infants can respond to several antigens as well as when responding to single stimuli. Current immunization schedules have been developed and tested to avoid vaccine interference, improve benefits and reduce side effects compared to single administrations. The infant immune system is therefore capable, early after birth, of managing several antigenic challenges and exploits them to prompt its development.
[Mh] Termos MeSH primário: Imunização/psicologia
Pais/psicologia
Vacinas/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Criança
Conhecimentos, Atitudes e Prática em Saúde
Seres Humanos
Imunidade Inata
Imunização/efeitos adversos
Esquemas de Imunização
Lactente
Mortalidade Infantil
Vacinas/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Vaccines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  9 / 42504 MEDLINE  
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[PMID]:29422654
[Au] Autor:Marcou Q; Mora T; Walczak AM
[Ad] Endereço:Laboratoire de Physique Théorique, CNRS, Sorbonne Université and École Normale Supérieure (PSL), 24, Rue Lhomond, 75005, Paris, France.
[Ti] Título:High-throughput immune repertoire analysis with IGoR.
[So] Source:Nat Commun;9(1):561, 2018 02 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:High-throughput immune repertoire sequencing is promising to lead to new statistical diagnostic tools for medicine and biology. Successful implementations of these methods require a correct characterization, analysis, and interpretation of these data sets. We present IGoR (Inference and Generation Of Repertoires)-a comprehensive tool that takes B or T cell receptor sequence reads and quantitatively characterizes the statistics of receptor generation from both cDNA and gDNA. It probabilistically annotates sequences and its modular structure can be used to investigate models of increasing biological complexity for different organisms. For B cells, IGoR returns the hypermutation statistics, which we use to reveal co-localization of hypermutations along the sequence. We demonstrate that IGoR outperforms existing tools in accuracy and estimate the sample sizes needed for reliable repertoire characterization.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos B/genética
Receptores de Antígenos de Linfócitos T/genética
Software
Linfócitos T/imunologia
Recombinação V(D)J
[Mh] Termos MeSH secundário: Linfócitos B/citologia
Sequência de Bases
Benchmarking
DNA Complementar/genética
DNA Complementar/imunologia
Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Imunidade Inata
Anotação de Sequência Molecular
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Linfócitos T/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180210
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02832-w


  10 / 42504 MEDLINE  
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Registro de Ensaios Clínicos
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[PMID]:28453702
[Au] Autor:Monk BJ; Brady MF; Aghajanian C; Lankes HA; Rizack T; Leach J; Fowler JM; Higgins R; Hanjani P; Morgan M; Edwards R; Bradley W; Kolevska T; Foukas P; Swisher EM; Anderson KS; Gottardo R; Bryan JK; Newkirk M; Manjarrez KL; Mannel RS; Hershberg RM; Coukos G
[Ad] Endereço:Arizona Oncology (US Oncology Network), University of Arizona, College of Medicine, Creighton University School of Medicine at St. Joseph's Hospital, Phoenix.
[Ti] Título:A phase 2, randomized, double-blind, placebo- controlled study of chemo-immunotherapy combination using motolimod with pegylated liposomal doxorubicin in recurrent or persistent ovarian cancer: a Gynecologic Oncology Group partners study.
[So] Source:Ann Oncol;28(5):996-1004, 2017 May 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: A phase 2, randomized, placebo-controlled trial was conducted in women with recurrent epithelial ovarian carcinoma to evaluate the efficacy and safety of motolimod-a Toll-like receptor 8 (TLR8) agonist that stimulates robust innate immune responses-combined with pegylated liposomal doxorubicin (PLD), a chemotherapeutic that induces immunogenic cell death. Patients and methods: Women with ovarian, fallopian tube, or primary peritoneal carcinoma were randomized 1 : 1 to receive PLD in combination with blinded motolimod or placebo. Randomization was stratified by platinum-free interval (≤6 versus >6-12 months) and Gynecologic Oncology Group (GOG) performance status (0 versus 1). Treatment cycles were repeated every 28 days until disease progression. Results: The addition of motolimod to PLD did not significantly improve overall survival (OS; log rank one-sided P = 0.923, HR = 1.22) or progression-free survival (PFS; log rank one-sided P = 0.943, HR = 1.21). The combination was well tolerated, with no synergistic or unexpected serious toxicity. Most patients experienced adverse events of fatigue, anemia, nausea, decreased white blood cells, and constipation. In pre-specified subgroup analyses, motolimod-treated patients who experienced injection site reactions (ISR) had a lower risk of death compared with those who did not experience ISR. Additionally, pre-treatment in vitro responses of immune biomarkers to TLR8 stimulation predicted OS outcomes in patients receiving motolimod on study. Immune score (tumor infiltrating lymphocytes; TIL), TLR8 single-nucleotide polymorphisms, mutational status in BRCA and other DNA repair genes, and autoantibody biomarkers did not correlate with OS or PFS. Conclusions: The addition of motolimod to PLD did not improve clinical outcomes compared with placebo. However, subset analyses identified statistically significant differences in the OS of motolimod-treated patients on the basis of ISR and in vitro immune responses. Collectively, these data may provide important clues for identifying patients for treatment with immunomodulatory agents in novel combinations and/or delivery approaches. Trial registration: Clinicaltrials.gov, NCT 01666444.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Recidiva Local de Neoplasia/tratamento farmacológico
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/administração & dosagem
Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Benzazepinas/administração & dosagem
Intervalo Livre de Doença
Método Duplo-Cego
Doxorrubicina/administração & dosagem
Doxorrubicina/análogos & derivados
Seres Humanos
Imunidade Inata/efeitos dos fármacos
Estimativa de Kaplan-Meier
Meia-Idade
Recidiva Local de Neoplasia/mortalidade
Neoplasias Epiteliais e Glandulares/mortalidade
Neoplasias Ovarianas/mortalidade
Polietilenoglicóis/administração & dosagem
Modelos de Riscos Proporcionais
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Benzazepines); 0 (VTX-2337); 0 (liposomal doxorubicin); 30IQX730WE (Polyethylene Glycols); 80168379AG (Doxorubicin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx049



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