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[PMID]:29223395
[Au] Autor:Takebe T; Sakamoto K; Higami Y; Harada Y
[Ad] Endereço:Laboratory of Pharmaceutical Immunology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba, 278-8510, Japan; Laboratory of Molecular Pathology and Metabolic Disease, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba,
[Ti] Título:A novel mouse model for tracking the fate of CXCR5-expressing T cells.
[So] Source:Biochem Biophys Res Commun;495(2):1642-1647, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The germinal center (GC) reaction, a critical process in the humoral immune response, requires follicular helper T (Tfh) cells. Tfh cells express the master transcription factor Bcl6 and chemokine receptor CXCR5, which enable them to migrate from the T cell zone to B cell follicles and interact with GC B cells. However, CXCR5 is downregulated when Tfh cells become memory cells. Therefore, it is difficult to track Tfh cells continuously in vivo. In this study, we generated a mouse strain, Cxcr5 R26 , in which the fluorescent protein tdTomato is inducibly expressed in CXCR5 cells by tamoxifen administration. After the oral administration of tamoxifen, most Tfh cells in Peyer's patches (PP) from Cxcr5 R26 mice were tdTomato . To track antigen-specific Tfh cells in vivo, OVA-specific OT-II T cells derived from Cxcr5 R26 mice were transferred to wild-type mice, and the recipient mice were immunized with OVA followed by tamoxifen administration. CXCR5 T cells became tdTomato and were mainly located in B cell follicles and GC areas 8 days after immunization. Four weeks after immunization, tdTomato OT-II T cells migrated from B cell follicles to the T-B border area and T cell zone after CXCR5 downregulation and CCR7 upregulation. These results indicate that Cxcr5 R26 mice are a useful tool for studying the cell fate of differentiated Tfh cells in vivo and therefore have implications for the development of therapeutic strategies for infectious and autoimmune diseases.
[Mh] Termos MeSH primário: Receptores CXCR5/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos B/imunologia
Diferenciação Celular
Movimento Celular/imunologia
Centro Germinativo/citologia
Centro Germinativo/imunologia
Imunidade Humoral
Memória Imunológica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Modelos Animais
Modelos Imunológicos
Ovalbumina/imunologia
Receptores CXCR5/genética
Linfócitos T Auxiliares-Indutores/citologia
Linfócitos T Auxiliares-Indutores/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blr1 protein, mouse); 0 (Receptors, CXCR5); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE


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[PMID]:28468795
[Au] Autor:Porcelijn L; Huiskes E; Schipperus M; van der Holt B; de Haas M; Zwaginga JJ; Dutch HOVON 64 Study Group
[Ad] Endereço:Immunohematology Diagnostics, Sanquin Diagnostic Services, Amsterdam, The Netherlands.
[Ti] Título:Lack of detectable platelet autoantibodies is correlated with nonresponsiveness to rituximab treatment in ITP patients.
[So] Source:Blood;129(25):3389-3391, 2017 06 22.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Plaquetas/imunologia
Púrpura Trombocitopênica Idiopática/tratamento farmacológico
Rituximab/uso terapêutico
[Mh] Termos MeSH secundário: Resistência a Medicamentos
Seres Humanos
Modelos Imunológicos
Plasmócitos/efeitos dos fármacos
Plasmócitos/imunologia
Púrpura Trombocitopênica Idiopática/sangue
Púrpura Trombocitopênica Idiopática/imunologia
Rituximab/farmacologia
Resultado do Tratamento
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Autoantibodies); 4F4X42SYQ6 (Rituximab)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-751719


  3 / 8904 MEDLINE  
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[PMID]:29304144
[Au] Autor:Davis CL; Wahid R; Toapanta FR; Simon JK; Sztein MB
[Ad] Endereço:Natural Science Division, Pepperdine University, Malibu, CA, United States of America.
[Ti] Título:A clinically parameterized mathematical model of Shigella immunity to inform vaccine design.
[So] Source:PLoS One;13(1):e0189571, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We refine and clinically parameterize a mathematical model of the humoral immune response against Shigella, a diarrheal bacteria that infects 80-165 million people and kills an estimated 600,000 people worldwide each year. Using Latin hypercube sampling and Monte Carlo simulations for parameter estimation, we fit our model to human immune data from two Shigella EcSf2a-2 vaccine trials and a rechallenge study in which antibody and B-cell responses against Shigella's lipopolysaccharide (LPS) and O-membrane proteins (OMP) were recorded. The clinically grounded model is used to mathematically investigate which key immune mechanisms and bacterial targets confer immunity against Shigella and to predict which humoral immune components should be elicited to create a protective vaccine against Shigella. The model offers insight into why the EcSf2a-2 vaccine had low efficacy and demonstrates that at a group level a humoral immune response induced by EcSf2a-2 vaccine or wild-type challenge against Shigella's LPS or OMP does not appear sufficient for protection. That is, the model predicts an uncontrolled infection of gut epithelial cells that is present across all best-fit model parameterizations when fit to EcSf2a-2 vaccine or wild-type challenge data. Using sensitivity analysis, we explore which model parameter values must be altered to prevent the destructive epithelial invasion by Shigella bacteria and identify four key parameter groups as potential vaccine targets or immune correlates: 1) the rate that Shigella migrates into the lamina propria or epithelium, 2) the rate that memory B cells (BM) differentiate into antibody-secreting cells (ASC), 3) the rate at which antibodies are produced by activated ASC, and 4) the Shigella-specific BM carrying capacity. This paper underscores the need for a multifaceted approach in ongoing efforts to design an effective Shigella vaccine.
[Mh] Termos MeSH primário: Modelos Imunológicos
Vacinas contra Shigella/imunologia
[Mh] Termos MeSH secundário: Anticorpos Antibacterianos/biossíntese
Linfócitos B/imunologia
Ensaios Clínicos como Assunto
Simulação por Computador
Desenho de Drogas
Disenteria Bacilar/imunologia
Disenteria Bacilar/microbiologia
Disenteria Bacilar/prevenção & controle
Interações Hospedeiro-Patógeno/imunologia
Seres Humanos
Imunidade Humoral
Conceitos Matemáticos
Método de Monte Carlo
Shigella/imunologia
Shigella/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Bacterial); 0 (Shigella Vaccines)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189571


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[PMID]:29253874
[Au] Autor:Martynov A; Severinov K; Ispolatov I
[Ad] Endereço:Center for Data-Intensive Biomedicine and Biotechnology, Skolkovo Institute of Science and Technology, Moscow, Russia.
[Ti] Título:Optimal number of spacers in CRISPR arrays.
[So] Source:PLoS Comput Biol;13(12):e1005891, 2017 12.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prokaryotic organisms survive under constant pressure of viruses. CRISPR-Cas system provides its prokaryotic host with an adaptive immune defense against viruses that have been previously encountered. It consists of two components: Cas-proteins that cleave the foreign DNA and CRISPR array that suits as a virus recognition key. CRISPR array consists of a series of spacers, short pieces of DNA that originate from and match the corresponding parts of viral DNA called protospacers. Here we estimate the number of spacers in a CRISPR array of a prokaryotic cell which maximizes its protection against a viral attack. The optimality follows from a competition between two trends: too few distinct spacers make host vulnerable to an attack by a virus with mutated corresponding protospacers, while an excessive variety of spacers dilutes the number of the CRISPR complexes armed with the most recent and thus most useful spacers. We first evaluate the optimal number of spacers in a simple scenario of an infection by a single viral species and later consider a more general case of multiple viral species. We find that depending on such parameters as the concentration of CRISPR-Cas interference complexes and its preference to arm with more recently acquired spacers, the rate of viral mutation, and the number of viral species, the predicted optimal number of spacers lies within a range that agrees with experimentally-observed values.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas
Repetições Palindrômicas Curtas Agrupadas e Regularmente Espaçadas/genética
[Mh] Termos MeSH secundário: Imunidade Adaptativa/genética
Archaea/genética
Archaea/imunologia
Archaea/virologia
Bactérias/genética
Bactérias/imunologia
Bactérias/virologia
Biologia Computacional
Simulação por Computador
DNA Intergênico/genética
DNA Viral/genética
Modelos Genéticos
Modelos Imunológicos
Mutação
Células Procarióticas/imunologia
Células Procarióticas/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Intergenic); 0 (DNA, Viral)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005891


  5 / 8904 MEDLINE  
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[PMID]:29242543
[Au] Autor:Nikolich-Zugich J
[Ad] Endereço:Department of Immunobiology and the Arizona Center on Aging, University of Arizona College of Medicine-Tucson, Tucson, AZ, USA. nikolich@email.arizona.edu.
[Ti] Título:The twilight of immunity: emerging concepts in aging of the immune system.
[So] Source:Nat Immunol;19(1):10-19, 2018 Jan.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunosenescence is a series of age-related changes that affect the immune system and, with time, lead to increased vulnerability to infectious diseases. This Review addresses recent developments in the understanding of age-related changes that affect key components of immunity, including the effect of aging on cells of the (mostly adaptive) immune system, on soluble molecules that guide the maintenance and function of the immune system and on lymphoid organs that coordinate both the maintenance of lymphocytes and the initiation of immune responses. I further address the effect of the metagenome and exposome as key modifiers of immune-system aging and discuss a conceptual framework in which age-related changes in immunity might also affect the basic rules by which the immune system operates.
[Mh] Termos MeSH primário: Imunidade Adaptativa/imunologia
Envelhecimento/imunologia
Sistema Imunitário/imunologia
Imunidade Inata/imunologia
[Mh] Termos MeSH secundário: Animais
Senescência Celular/imunologia
Seres Humanos
Linfócitos/imunologia
Linfócitos/metabolismo
Modelos Imunológicos
Receptores de Antígenos de Linfócitos T/imunologia
Receptores de Antígenos de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1038/s41590-017-0006-x


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[PMID]:29045898
[Au] Autor:Kleino A; Ramia NF; Bozkurt G; Shen Y; Nailwal H; Huang J; Napetschnig J; Gangloff M; Chan FK; Wu H; Li J; Silverman N
[Ad] Endereço:Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
[Ti] Título:Peptidoglycan-Sensing Receptors Trigger the Formation of Functional Amyloids of the Adaptor Protein Imd to Initiate Drosophila NF-κB Signaling.
[So] Source:Immunity;47(4):635-647.e6, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the Drosophila immune response, bacterial derived diaminopimelic acid-type peptidoglycan binds the receptors PGRP-LC and PGRP-LE, which through interaction with the adaptor protein Imd leads to activation of the NF-κB homolog Relish and robust antimicrobial peptide gene expression. PGRP-LC, PGRP-LE, and Imd each contain a motif with some resemblance to the RIP Homotypic Interaction Motif (RHIM), a domain found in mammalian RIPK proteins forming functional amyloids during necroptosis. Here we found that despite sequence divergence, these Drosophila cryptic RHIMs formed amyloid fibrils in vitro and in cells. Amyloid formation was required for signaling downstream of Imd, and in contrast to the mammalian RHIMs, was not associated with cell death. Furthermore, amyloid formation constituted a regulatable step and could be inhibited by Pirk, an endogenous feedback regulator of this pathway. Thus, diverse sequence motifs are capable of forming amyloidal signaling platforms, and the formation of these platforms may present a regulatory point in multiple biological processes.
[Mh] Termos MeSH primário: Amiloide/imunologia
Proteínas de Transporte/imunologia
Proteínas de Drosophila/imunologia
NF-kappa B/imunologia
Receptores de Superfície Celular/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Motivos de Aminoácidos/genética
Motivos de Aminoácidos/imunologia
Sequência de Aminoácidos
Amiloide/metabolismo
Animais
Sítios de Ligação/genética
Sítios de Ligação/imunologia
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Linhagem Celular
Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/citologia
Drosophila melanogaster/genética
Drosophila melanogaster/imunologia
Feminino
Expressão Gênica/imunologia
Masculino
Microscopia Confocal
Modelos Imunológicos
Mutação
NF-kappa B/metabolismo
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/imunologia
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Receptores de Superfície Celular/genética
Receptores de Superfície Celular/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Homologia de Sequência de Aminoácidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid); 0 (Carrier Proteins); 0 (Drosophila Proteins); 0 (NF-kappa B); 0 (Receptors, Cell Surface); 0 (immune deficiency protein, Drosophila); 0 (peptidoglycan receptor); 0 (peptidoglycan recognition protein); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE


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[PMID]:29045897
[Au] Autor:Tabas I; Lichtman AH
[Ad] Endereço:Departments of Medicine, Physiology, and Pathology & Cell Biology, Columbia University Medical Center, New York, NY 10032, USA. Electronic address: iat1@columbia.edu.
[Ti] Título:Monocyte-Macrophages and T Cells in Atherosclerosis.
[So] Source:Immunity;47(4):621-634, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is an arterial disease process characterized by the focal subendothelial accumulation of apolipoprotein-B-containing lipoproteins, immune and vascular wall cells, and extracellular matrix. The lipoproteins acquire features of damage-associated molecular patterns and trigger first an innate immune response, dominated by monocyte-macrophages, and then an adaptive immune response. These inflammatory responses often become chronic and non-resolving and can lead to arterial damage and thrombosis-induced organ infarction. The innate immune response is regulated at various stages, from hematopoiesis to monocyte changes and macrophage activation. The adaptive immune response is regulated primarily by mechanisms that affect the balance between regulatory and effector T cells. Mechanisms related to cellular cholesterol, phenotypic plasticity, metabolism, and aging play key roles in affecting these responses. Herein, we review select topics that shed light on these processes and suggest new treatment strategies.
[Mh] Termos MeSH primário: Aterosclerose/imunologia
Macrófagos/imunologia
Monócitos/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Animais
Seres Humanos
Imunidade Inata/imunologia
Lipoproteínas/imunologia
Modelos Imunológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Lipoproteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE


  8 / 8904 MEDLINE  
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[PMID]:29044230
[Au] Autor:De Rosa V; La Cava A; Matarese G
[Ad] Endereço:Laboratorio di Immunologia, Istituto per l'Endocrinologia e l'Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, Napoli, Italy.
[Ti] Título:Metabolic pressure and the breach of immunological self-tolerance.
[So] Source:Nat Immunol;18(11):1190-1196, 2017 Oct 18.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The prevalence of autoimmune disorders in affluent countries has reached epidemic proportions. Over the past 50 years, a reverse trend between the frequency of infectious diseases and the incidence of autoimmune and allergic diseases led to the so-called 'hygiene hypothesis'. Given the epidemiological evidence and recent experimental data, we propose that this concept should also include metabolic pressure secondary to exposure to excessive daily caloric intake and overnutrition. We discuss how metabolic workload can modulate immunological tolerance and review the molecular mechanisms and the state of the art of the field. We also critically evaluate possibilities for restoring immunological homeostasis under conditions of metabolic pressure.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Doenças Autoimunes/metabolismo
Homeostase/imunologia
Hipótese da Higiene
Tolerância a Antígenos Próprios/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Redes e Vias Metabólicas/imunologia
Modelos Imunológicos
Fenômenos Fisiológicos da Nutrição/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3851


  9 / 8904 MEDLINE  
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[PMID]:28988040
[Au] Autor:Marino R; Capoferri R; Panelli S; Minozzi G; Strozzi F; Trevisi E; Snel GGM; Ajmone-Marsan P; Williams JL
[Ad] Endereço:CREA Research Centre for Animal Production and Aquaculture, Via Antonio Lombardo 11, 26900 Lodi, Italy; Istituto Sperimentale Italiano "Lazzaro Spallanzani", 26027, Rivolta d'Adda, Cremona, Italy; Institute of Zootechnics, Università Cattolica del S. Cuore, Via Emilia Parmense 84, 29122 Piacenza, It
[Ti] Título:Johne's disease in cattle: an in vitro model to study early response to infection of Mycobacterium avium subsp. paratuberculosis using RNA-seq.
[So] Source:Mol Immunol;91:259-271, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Johne's disease is a chronic granulomatous enteritis caused by Mycobacterium avium subsp. paratubercolosis (MAP) which affects ruminants worldwide and has a significant economic impact. MAP has also been associated with human Crohn's disease, although this connection is not well established. MAP is highly adapted for survival within host macrophages and prevents macrophage activation, blocks phagosome acidification and maturation, and attenuates presentation of antigens to the immune system. The consequence is a very long silent infection before clinical signs are observed. The present work examined the transcriptome of bovine monocyte-derived macrophages (MDM) infected with the L1 strain of MAP at 2h, 6h and 24h post infection using RNA-seq. Pathway over-representation analysis of genes differentially expressed between infected vs. control MDM identified that immune related pathways were affected. Genes belonging to the cytokine-cytokine receptor interaction pathway and members of the JAK-STAT pathway, which is involved in the regulation of immune response, were up-regulated. However, in parallel inhibitors of immune functions were activated, including suppressor of cytokine signaling (SOCS) and cytokine-inducible SH2-containing protein (CISH), which most likely suppresses IFNγ and the JAK/STAT signaling cascade in infected MDM, which may favour MAP survival. After exposure, macrophages phagocytise pathogens, activate the complement cascade and the adaptive immune system through the antigen presentation process. However, data presented here suggest that genes related to phagocytosis and lysosome function are down regulated in MAP infected MDM. Genes of MHC class II and complement pathway were also down-regulated. This study therefore shows that MAP infection is associated with changes in expression of genes related to the host immune response that may affect its ability to survive and multiply inside the host cell.
[Mh] Termos MeSH primário: Doenças dos Bovinos/imunologia
Regulação da Expressão Gênica/imunologia
Macrófagos/imunologia
Modelos Imunológicos
Mycobacterium avium subsp. paratuberculosis/imunologia
Paratuberculose/imunologia
Transcriptoma/imunologia
[Mh] Termos MeSH secundário: Animais
Bovinos
Doenças dos Bovinos/microbiologia
Doenças dos Bovinos/patologia
Feminino
Macrófagos/microbiologia
Macrófagos/patologia
Paratuberculose/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


  10 / 8904 MEDLINE  
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[PMID]:28910616
[Au] Autor:Jassam YN; Izzy S; Whalen M; McGavern DB; El Khoury J
[Ad] Endereço:National Institute of Neurological Disorders and Stroke (NINDS), NIH, Bethesda, MD 20892, USA.
[Ti] Título:Neuroimmunology of Traumatic Brain Injury: Time for a Paradigm Shift.
[So] Source:Neuron;95(6):1246-1265, 2017 Sep 13.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Traumatic brain injury (TBI) is a leading cause of morbidity and disability, with a considerable socioeconomic burden. Heterogeneity of pathoanatomical subtypes and diversity in the pathogenesis and extent of injury contribute to differences in the course and outcome of TBI. Following the primary injury, extensive and lasting damage is sustained through a complex cascade of events referred to as "secondary injury." Neuroinflammation is proposed as an important manipulable aspect of secondary injury in animal and human studies. Because neuroinflammation can be detrimental or beneficial, before developing immunomodulatory therapies, it is necessary to better understand the timing and complexity of the immune responses that follow TBI. With a rapidly increasing body of literature, there is a need for a clear summary of TBI neuroimmunology. This review presents our current understanding of the immune response to TBI in a chronological and compartment-based manner, highlighting early changes in gene expression and initial signaling pathways that lead to activation of innate and adaptive immunity. Based on recent advances in our understanding of innate immune cell activation, we propose a new paradigm to study innate immune cells following TBI that moves away from the existing M1/M2 classification of activation states toward a stimulus- and disease-specific understanding of polarization state based on transcriptomic and proteomic profiling.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/imunologia
Lesões Encefálicas Traumáticas/patologia
Inflamação/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Astrócitos/imunologia
Lesões Encefálicas Traumáticas/complicações
Lesões Encefálicas Traumáticas/genética
Seres Humanos
Imunidade Inata
Inflamação/complicações
Inflamação/patologia
Microglia/imunologia
Modelos Imunológicos
Proteômica
Transcriptoma/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE



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