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[PMID]:28707669
[Au] Autor:Cortés A; Coral J; McLachlan C; Benítez R; Pinilla L
[Ad] Endereço:Department of Molecular Physics, Synthetic Vaccine and New Drug Research Institute, IVSI, Popayán, Colombia.
[Ti] Título:[Planar molecular arrangements aid the design of MHC class II binding peptides].
[So] Source:Mol Biol (Mosk);51(3):524-533, 2017 May-Jun.
[Is] ISSN:0026-8984
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The coupling between peptides and MHC-II proteins in the human immune system is not well understood. This work presents an evidence-based hypothesis of a guiding intermolecular force present in every human MHC-II protein (HLA-II). Previously, we examined the spatial positions of the fully conserved residues in all HLA-II protein types. In each one, constant planar patterns were revealed. These molecular planes comprise of amino acid groups of the same chemical species (for example, Gly) distributed across the protein structure. Each amino acid plane has a unique direction and this directional element offers spatial selectivity. Constant within all planes, too, is the presence of an aromatic residue possessing electrons in movement, leading the authors to consider that the planes generate electromagnetic fields that could serve as an attractive force in a single direction. Selection and attraction between HLA-II molecules and antigen peptides would, therefore, be non-random, resulting in a coupling mechanism as effective and rapid as is clearly required in the immune response. On the basis of planar projections onto the HLA-II groove, modifications were made by substituting the key residues in the class II-associated invariant chain peptide-a peptide with a universal binding affinity-resulting in eight different modified peptides with affinities greater than that of the unmodified peptide. Accurate and reliable prediction of MHC class II-binding peptides may facilitate the design of universal vaccine-peptides with greatly enhanced binding affinities. The proposed mechanisms of selection, attraction and coupling between HLA-II and antigen peptides are explained further in the paper.
[Mh] Termos MeSH primário: Epitopos/metabolismo
Antígenos HLA/metabolismo
Oligopeptídeos/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos/genética
Aminoácidos/química
Aminoácidos/imunologia
Antígenos de Diferenciação de Linfócitos B/química
Antígenos de Diferenciação de Linfócitos B/imunologia
Sítios de Ligação
Epitopos/química
Epitopos/imunologia
Antígenos HLA/química
Antígenos HLA/imunologia
Antígenos de Histocompatibilidade Classe II/química
Antígenos de Histocompatibilidade Classe II/imunologia
Seres Humanos
Conformação Molecular
Oligopeptídeos/química
Oligopeptídeos/imunologia
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (Epitopes); 0 (HLA Antigens); 0 (Histocompatibility Antigens Class II); 0 (MHC binding peptide); 0 (Oligopeptides); 0 (invariant chain)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.7868/S0026898417020082


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[PMID]:28671983
[Au] Autor:Du X; Jiang C; Lv Y; Dull RO; Zhao YY; Schwartz DE; Hu G
[Ad] Endereço:Department of Anesthesiology, University of Illinois College of Medicine, Chicago, Illinois, United States of America.
[Ti] Título:Isoflurane promotes phagocytosis of apoptotic neutrophils through AMPK-mediated ADAM17/Mer signaling.
[So] Source:PLoS One;12(7):e0180213, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A patient's recovery from lung inflammatory injury or development of multi-system organ failure is determined by the host's ability to resolve inflammation and repair tissue damage, both of which require the clearance of apoptotic neutrophils by macrophages (efferocytosis). Here, we investigated the effects of isoflurane on macrophage efferocytosis and resolution of lung inflammatory injury. Treatment of murine bone marrow-derived macrophages (BMDMs) or alveolar macrophages with isoflurane dramatically enhanced phagocytosis of apoptotic neutrophils. Isoflurane significantly increased the surface expression of the receptor tyrosine kinase Mer in macrophages, but markedly decreased the levels of a soluble form of Mer protein in the medium. Isoflurane treatment also caused a decrease in a disintegrin and metalloproteinase 17 (ADAM17) on the cell surface and a concomitant increase in its cytoplasmic fraction. These responses induced by isoflurane were completely reversed by a pharmacological inhibitor or genetic deletion of AMP-activated protein kinase (AMPK). In a mouse model of lipopolysaccharide-induced lung injury, isoflurane accelerated the recovery of lung inflammation and injury that was coupled with an increase in the number of alveolar macrophages containing apoptotic bodies. In alveolar macrophage-depleted mice, administration of isoflurane-pretreated BMDMs facilitated resolution of lung inflammation following lipopolysaccharide challenge. Thus, isoflurane promoted resolution of lipopolysaccharide-induced lung inflammatory injury via enhancement of macrophage efferocytosis. Increased macrophage efferocytosis following isoflurane treatment correlates with upregulation of Mer surface expression through AMPK-mediated blockade of ADAM17 trafficking to the cell membrane.
[Mh] Termos MeSH primário: Proteína ADAM17/metabolismo
Proteínas Quinases Ativadas por AMP/metabolismo
Antígenos de Diferenciação de Linfócitos B/metabolismo
Apoptose
Isoflurano/farmacologia
Neutrófilos/efeitos dos fármacos
Fagocitose/efeitos dos fármacos
Receptores Imunológicos/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Lesão Pulmonar Aguda/induzido quimicamente
Animais
Células Cultivadas
Técnicas de Silenciamento de Genes
Lipopolissacarídeos/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Neutrófilos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, B-Lymphocyte); 0 (Lipopolysaccharides); 0 (Receptors, Immunologic); 0 (mouse erythrocyte receptor); CYS9AKD70P (Isoflurane); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.4.24.86 (ADAM17 Protein)
[Em] Mês de entrada:1710
[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:10.1371/journal.pone.0180213


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[PMID]:28642294
[Au] Autor:Chatterjee P; Chiasson VL; Seerangan G; De Guzman E; Milad M; Bounds KR; Gasheva O; Tobin RP; Hatahet M; Kopriva S; Jones KA; Newell-Rogers MK; Mitchell BM
[Ad] Endereço:Department of Internal Medicine, Texas A&M University Health Science Center/Baylor Scott and White Health, 702 SW HK Dodgen Loop, Temple, Texas 76504, U.S.A.
[Ti] Título:Depletion of MHC class II invariant chain peptide or γ-δ T-cells ameliorates experimental preeclampsia.
[So] Source:Clin Sci (Lond);131(15):2047-2058, 2017 08 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Excessive innate immune system activation and inflammation during pregnancy can lead to organ injury and dysfunction and preeclampsia (PE); however, the molecular mechanisms involved are unknown. We tested the hypothesis that Toll-like receptor (TLR) activation induces major histocompatibility complex (MHC) class II invariant chain peptide (CLIP) expression on immune cells, makes them pro-inflammatory, and are necessary to cause PE-like features in mice. Treatment with VG1177, a competitive antagonist peptide for CLIP in the groove of MHC class II, was able to both prevent and treat PE-like features in mice. We then determined that γ-δ T cells are critical for the development of PE-like features in mice since γ-δ T-cell knockout mice, like CLIP deficient mice, are resistant to developing PE-like features. Placentas from women with PE exhibit significantly increased levels of γ-δ T cells. These preclinical data demonstrate that CLIP expression and activated γ-δ T cells are responsible for the development of immunologic PE-like features and that temporarily antagonizing CLIP and/or γ-δ T cells may be a therapeutic strategy for PE.
[Mh] Termos MeSH primário: Antígenos de Diferenciação de Linfócitos B/genética
Genes MHC Classe II
Antígenos de Histocompatibilidade Classe II/genética
Pré-Eclâmpsia/genética
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação de Linfócitos B/imunologia
Feminino
Antígenos de Histocompatibilidade Classe II/imunologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Pré-Eclâmpsia/imunologia
Gravidez
Receptores Toll-Like
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, B-Lymphocyte); 0 (Histocompatibility Antigens Class II); 0 (Toll-Like Receptors); 0 (invariant chain)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1042/CS20171008


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[PMID]:28628828
[Au] Autor:Varela M; Piras IM; Mullan C; Shi X; Tilston-Lunel NL; Pinto RM; Taggart A; Welch SR; Neil SJD; Kreher F; Elliott RM; Palmarini M
[Ad] Endereço:MRC-University of Glasgow Centre for Virus Research, 464 Bearsden Road, Glasgow G61 1QH, Scotland, United Kingdom. Electronic address: mariana.varela@glasgow.ac.uk.
[Ti] Título:Sensitivity to BST-2 restriction correlates with Orthobunyavirus host range.
[So] Source:Virology;509:121-130, 2017 Sep.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Orthobunyaviruses include several recently emerging viruses of significant medical and veterinary importance. There is currently very limited understanding on what determines the host species range of these pathogens. In this study we discovered that BST-2/tetherin restricts orthobunyavirus replication in a host-specific manner. We show that viruses with human tropism (Oropouche virus and La Crosse virus) are restricted by sheep BST-2 but not by the human orthologue, while viruses with ruminant tropism (Schmallenberg virus and others) are restricted by human BST-2 but not by the sheep orthologue. We also show that BST-2 blocks orthobunyaviruses replication by reducing the amount of envelope glycoprotein into viral particles egressing from infected cells. This is the first study identifying a restriction factor that correlates with species susceptibility to orthobunyavirus infection. This work provides insight to help us dissect the adaptive changes that bunyaviruses require to cross the species barrier and emerge into new species.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Antígenos de Diferenciação de Linfócitos B/metabolismo
Especificidade de Hospedeiro
Interações Hospedeiro-Patógeno
Orthobunyavirus/imunologia
Orthobunyavirus/fisiologia
Proteínas do Envelope Viral/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Proteínas Ligadas por GPI/metabolismo
Seres Humanos
Ovinos
Liberação de Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (BST2 protein, human); 0 (GPI-Linked Proteins); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


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[PMID]:28597514
[Au] Autor:Ranganathan V; Ciccia F; Zeng F; Sari I; Guggino G; Muralitharan J; Gracey E; Haroon N
[Ti] Título:Macrophage Migration Inhibitory Factor Induces Inflammation and Predicts Spinal Progression in Ankylosing Spondylitis.
[So] Source:Arthritis Rheumatol;69(9):1796-1806, 2017 Sep.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To investigate the role of macrophage migration inhibitory factor (MIF) in the pathogenesis of ankylosing spondylitis (AS). METHODS: Patients who met the modified New York criteria for AS were recruited for the study. Healthy volunteers, rheumatoid arthritis patients, and osteoarthritis patients were included as controls. Based on the annual rate of increase in modified Stoke AS Spine Score (mSASSS), AS patients were classified as progressors or nonprogressors. MIF levels in serum and synovial fluid were quantitated by enzyme-linked immunosorbent assay. Predictors of AS progression were evaluated using logistic regression analysis. Immunohistochemical analysis of ileal tissue was performed to identify MIF-producing cells. Flow cytometry was used to identify MIF-producing subsets, expression patterns of the MIF receptor (CD74), and MIF-induced tumor necrosis factor (TNF) production in the peripheral blood. MIF-induced mineralization of osteoblast cells (SaOS-2) was analyzed by alizarin red S staining, and Western blotting was used to quantify active ß-catenin levels. RESULTS: Baseline serum MIF levels were significantly elevated in AS patients compared to healthy controls and were found to independently predict AS progression. MIF levels were higher in the synovial fluid of AS patients, and MIF-producing macrophages and Paneth cells were enriched in their gut. MIF induced TNF production in monocytes, activated ß-catenin in osteoblasts, and promoted the mineralization of osteoblasts. CONCLUSION: Our findings indicate an unexplored pathogenic role of MIF in AS and a link between inflammation and new bone formation.
[Mh] Termos MeSH primário: Progressão da Doença
Oxirredutases Intramoleculares/análise
Fatores Inibidores da Migração de Macrófagos/análise
Espondilite Anquilosante/imunologia
Espondilite Anquilosante/patologia
[Mh] Termos MeSH secundário: Adulto
Antígenos de Diferenciação de Linfócitos B/sangue
Calcificação Fisiológica
Estudos de Casos e Controles
Ensaio de Imunoadsorção Enzimática
Feminino
Antígenos de Histocompatibilidade Classe II/sangue
Seres Humanos
Modelos Logísticos
Macrófagos/metabolismo
Masculino
Meia-Idade
Monócitos/metabolismo
Osteoblastos/patologia
Celulas de Paneth/metabolismo
Valor Preditivo dos Testes
Índice de Gravidade de Doença
Coluna Vertebral/imunologia
Coluna Vertebral/patologia
Espondilite Anquilosante/sangue
Líquido Sinovial/química
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, B-Lymphocyte); 0 (Histocompatibility Antigens Class II); 0 (Macrophage Migration-Inhibitory Factors); 0 (Tumor Necrosis Factor-alpha); 0 (invariant chain); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (MIF protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1002/art.40175


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[PMID]:28550201
[Au] Autor:Schneppenheim J; Loock AC; Hüttl S; Schweizer M; Lüllmann-Rauch R; Oberg HH; Arnold P; Lehmann CHK; Dudziak D; Kabelitz D; Lucius R; Lennon-Duménil AM; Saftig P; Schröder B
[Ad] Endereço:Biochemical Institute, Christian-Albrechts-University of Kiel, D-24118 Kiel, Germany.
[Ti] Título:The Influence of MHC Class II on B Cell Defects Induced by Invariant Chain/CD74 N-Terminal Fragments.
[So] Source:J Immunol;199(1):172-185, 2017 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The invariant chain (CD74) mediates assembly and targeting of MHC class II (MHCII) complexes. In endosomes, CD74 undergoes sequential degradation by different proteases, including cathepsin S (CatS) and the intramembrane protease signal peptide peptidase-like 2a (SPPL2a). In their absence, CD74 N-terminal fragments (NTFs) accumulate. In B cells, such an NTF impairs endosomal trafficking and BCR signal transduction. In mice, this leads to a loss of splenic B cells beyond the transitional stage 1. To gain insight into CD74 determinants and the role of MHCII, we compared B cells from , , and SPPL2a-MHCII double-deficient mice. We assessed differentiation of B cells in bone marrow and spleen and analyzed their endosomal morphology, BCR expression, and signal transduction. We demonstrate that MHCII is dispensable for the B cell phenotype of mice, further supporting a CD74-intrinsic effect. Despite significant vacuolization of endosomal compartments similar to B cells, traditional stage 1 B cells show unimpaired degradation of endocytic cargo, have intact BCR signaling, and do not exhibit any relevant defects in maturation. This could indicate that CD74 NTF-induced structural changes of endosomes are not directly involved in these processes. We further found that the block of CD74 degradation in B cells is incomplete, so that NTF levels are significantly lower than in B cells. This suggests a dose dependency and threshold for the CD74 NTF-associated impairment of B cell signaling and maturation. In addition, different functional properties of the longer, MHCII-bound CD74 NTF could contribute to the milder phenotype of B cells.
[Mh] Termos MeSH primário: Antígenos de Diferenciação de Linfócitos B/imunologia
Linfócitos B/imunologia
Genes MHC Classe II
Antígenos de Histocompatibilidade Classe II/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação de Linfócitos B/metabolismo
Ácido Aspártico Endopeptidases/deficiência
Ácido Aspártico Endopeptidases/genética
Ácido Aspártico Endopeptidases/metabolismo
Catepsinas/deficiência
Catepsinas/genética
Catepsinas/metabolismo
Diferenciação Celular
Endossomos/imunologia
Endossomos/fisiologia
Antígenos de Histocompatibilidade Classe II/metabolismo
Proteínas de Membrana/deficiência
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, B-Lymphocyte); 0 (Histocompatibility Antigens Class II); 0 (Membrane Proteins); 0 (invariant chain); EC 3.4.- (Cathepsins); EC 3.4.22.27 (cathepsin S); EC 3.4.23.- (Aspartic Acid Endopeptidases); EC 3.4.23.- (SPPL2a protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601533


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[PMID]:28539339
[Au] Autor:Ochi A; Chen D; Schulte W; Leng L; Moeckel N; Piecychna M; Averdunk L; Stoppe C; Bucala R; Moeckel G
[Ad] Endereço:Department of Pathology, Yale University School of Medicine, New Haven, Connecticut.
[Ti] Título:MIF-2/D-DT enhances proximal tubular cell regeneration through SLPI- and ATF4-dependent mechanisms.
[So] Source:Am J Physiol Renal Physiol;313(3):F767-F780, 2017 Sep 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macrophage migration inhibitory factor (MIF) is a cytokine with pleiotropic actions that is produced by several organs and cell types. Depending on the target cell and the inflammatory context, MIF can engage its two component receptor complex CD74 and CD44 and the chemokine receptors CXCR2/4. MIF is constitutively expressed in renal proximal tubular cells, stored in intracellular preformed pools, and released at a low rate. Recently, a second MIF-like protein (i.e., MIF-2/D-DT) has been characterized in mammals. Our study was aimed at examining the role of MIF-2/D-DT, which mediates tissue protection in the heart, in tubular cell regeneration from ischemia-reperfusion injury. We found that , , and mice had significantly worse tubular injury compared with wild-type (WT) control mice and that treatment with MIF-2/D-DT significantly improved recovery of injured epithelial cells. RNAseq analysis of kidney tissue from the ischemia-reperfusion injury model revealed that MIF-2/D-DT treatment stimulates secretory leukocyte proteinase inhibitor (SLPI) and cyclin D1 expression. MIF-2/D-DT additionally activates of eukaryotic initiation factor (eIF) 2α and activating transcription factor (ATF) 4, two transcription factors involved in the integrated stress response (ISR), which is a cellular stress response activated by hypoxia, nutrient deprivation, and oxygen radicals. MIF-2/D-DT also inhibited apoptosis and induced autophagy in hypoxia-treated mouse proximal tubular (MPT) cells. These results indicate that MIF-2/D-DT is an important factor in tubular cell regeneration and may be of therapeutic utility as a regenerative agent in the clinical setting of ischemic acute kidney injury.
[Mh] Termos MeSH primário: Fator 4 Ativador da Transcrição/metabolismo
Lesão Renal Aguda/metabolismo
Proliferação Celular
Oxirredutases Intramoleculares/metabolismo
Túbulos Renais Proximais/metabolismo
Regeneração
Traumatismo por Reperfusão/metabolismo
Inibidor Secretado de Peptidases Leucocitárias/metabolismo
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/deficiência
Fator 4 Ativador da Transcrição/genética
Lesão Renal Aguda/patologia
Lesão Renal Aguda/fisiopatologia
Lesão Renal Aguda/prevenção & controle
Animais
Antígenos de Diferenciação de Linfócitos B/genética
Antígenos de Diferenciação de Linfócitos B/metabolismo
Apoptose
Autofagia
Hipóxia Celular
Linhagem Celular
Ciclina D1/metabolismo
Modelos Animais de Doenças
Fator de Iniciação 2 em Eucariotos/metabolismo
Feminino
Predisposição Genética para Doença
Antígenos de Histocompatibilidade Classe II/genética
Antígenos de Histocompatibilidade Classe II/metabolismo
Oxirredutases Intramoleculares/deficiência
Oxirredutases Intramoleculares/genética
Túbulos Renais Proximais/patologia
Túbulos Renais Proximais/fisiopatologia
Fatores Inibidores da Migração de Macrófagos/genética
Fatores Inibidores da Migração de Macrófagos/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Traumatismo por Reperfusão/patologia
Traumatismo por Reperfusão/fisiopatologia
Traumatismo por Reperfusão/prevenção & controle
Inibidor Secretado de Peptidases Leucocitárias/genética
Transdução de Sinais
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, B-Lymphocyte); 0 (Atf4 protein, mouse); 0 (Ccnd1 protein, mouse); 0 (Eukaryotic Initiation Factor-2); 0 (Histocompatibility Antigens Class II); 0 (Macrophage Migration-Inhibitory Factors); 0 (Secretory Leukocyte Peptidase Inhibitor); 0 (Slpi protein, mouse); 0 (invariant chain); 136601-57-5 (Cyclin D1); 145891-90-3 (Activating Transcription Factor 4); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (Mif protein, mouse); EC 5.3.3.12 (dopachrome isomerase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00683.2016


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[PMID]:28419421
[Au] Autor:Lyu M; Hao Y; Li Y; Lyu C; Liu W; Li H; Xue F; Liu X; Yang R
[Ad] Endereço:State Key Laboratory of Experimental Haematology, Institute of Haematology and Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
[Ti] Título:Upregulation of CD72 expression on CD19 CD27 memory B cells by CD40L in primary immune thrombocytopenia.
[So] Source:Br J Haematol;178(2):308-318, 2017 Jul.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CD72 is a co-receptor of B cells and regulates B cell activation. Although aberrant expression of CD72 has been reported in primary immune thrombocytopenia (ITP), it is uncertain whether this aberrant expression is restricted to specific B cell subsets. Furthermore, the mechanisms that regulate CD72 expression are unknown. In this study, we found higher frequency of CD19 B cells, CD19 CD27 memory B cells and lower frequency of CD19 CD27 naive B cells in active ITP patients compared with controls and patients in remission. CD72 expression on CD19 CD27 cells was upregulated in active ITP patients and correlated with platelet count and anti-platelet autoantibodies. In vitro, CD40L could specifically induce CD72 upregulation on CD19 CD27 B cells. In combination with CD40L, interleukin (IL) 10 and BAFF (also termed TNFSF13B) further enhanced CD72 expression on CD19 CD27 B cells, whereas IL21 reduced CD72 upregulation. CD72mRNA expression after CD40L stimulation was increased in ITP patients and controls. Significant increase of CD40L on CD4 T cells was correlated with CD72 expression on CD19 CD27 B cells in ITP patients. In conclusion, upregulation of CD72 expression on CD27 memory B cells might take part in the pathogenesis of ITP. Elevated CD40L on CD4 cells combined with cytokines might contribute to the upregulation of CD72 expression on CD27 memory B cells.
[Mh] Termos MeSH primário: Antígenos CD19/metabolismo
Antígenos CD/metabolismo
Antígenos de Diferenciação de Linfócitos B/metabolismo
Linfócitos B/imunologia
Ligante de CD40/metabolismo
Púrpura Trombocitopênica Idiopática/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Adulto
Fator Ativador de Células B/farmacologia
Subpopulações de Linfócitos B/imunologia
Ligante de CD40/farmacologia
Estudos de Casos e Controles
Células Cultivadas
Feminino
Seres Humanos
Memória Imunológica/fisiologia
Interleucina-10/farmacologia
Interleucinas/farmacologia
Masculino
Meia-Idade
Regulação para Cima/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, CD19); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (B-Cell Activating Factor); 0 (CD72 protein, human); 0 (Interleukins); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-21); 130068-27-8 (Interleukin-10); 147205-72-9 (CD40 Ligand)
[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:170419
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14671


  9 / 4234 MEDLINE  
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[PMID]:28363897
[Au] Autor:Kräutler NJ; Suan D; Butt D; Bourne K; Hermes JR; Chan TD; Sundling C; Kaplan W; Schofield P; Jackson J; Basten A; Christ D; Brink R
[Ad] Endereço:Immunology Division, Garvan Institute of Medical Research, Darlinghurst NSW 2010, Australia.
[Ti] Título:Differentiation of germinal center B cells into plasma cells is initiated by high-affinity antigen and completed by Tfh cells.
[So] Source:J Exp Med;214(5):1259-1267, 2017 May 01.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasma cells (PCs) derived from germinal centers (GCs) secrete the high-affinity antibodies required for long-term serological immunity. Nevertheless, the process whereby GC B cells differentiate into PCs is uncharacterized, and the mechanism underlying the selective PC differentiation of only high-affinity GC B cells remains unknown. In this study, we show that differentiation into PCs is induced among a discrete subset of high-affinity B cells residing within the light zone of the GC. Initiation of differentiation required signals delivered upon engagement with intact antigen. Signals delivered by T follicular helper cells were not required to initiate differentiation but were essential to complete the differentiation process and drive migration of maturing PCs through the dark zone and out of the GC. This bipartite or two-signal mechanism has likely evolved to both sustain protective immunity and avoid autoantibody production.
[Mh] Termos MeSH primário: Antígenos de Diferenciação de Linfócitos B/fisiologia
Linfócitos B/fisiologia
Diferenciação Celular/fisiologia
Centro Germinativo/fisiologia
Plasmócitos/fisiologia
Linfócitos T Auxiliares-Indutores/fisiologia
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, B-Lymphocyte)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170402
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161533


  10 / 4234 MEDLINE  
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[PMID]:28222623
[Au] Autor:Li BJ; He Y; Zhang Y; Guo YH; Zhou Y; Zhang PX; Wang W; Zhao JR; Li JG; Zuo WZ; Fan C; Jia ZS
[Ad] Endereço:2 First Affiliated Hospital, School of Medicine, Shihezi University, Xinjiang, China.
[Ti] Título:Interferon-α-induced CD100 on naïve CD8 T cells enhances antiviral responses to hepatitis C infection through CD72 signal transduction.
[So] Source:J Int Med Res;45(1):89-100, 2017 Feb.
[Is] ISSN:1473-2300
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives We investigated the effects of CD100 on naïve CD8 T cells during hepatitis C virus (HCV) infection after interferon-α (IFN-α) therapy to clarify the mechanism underlying the effect of IFN-α in enhancing the antiviral response. Methods The CD100 molecules on subsets of CD8 T cells were analysed with flow cytometry. The effects of CD100-overexpressing naïve CD8 T cells were determined with ELISAs and an MTT cytotoxicity assay. The role of CD100-CD72 signal transduction was analysed with a neutralization and transwell assays. Results HCV infection reduced CD100 expression on CD8 T cells, whereas IFN-α treatment significantly increased CD100 expression on naïve CD8 T cells. The increased CD100 interacted with the CD72 receptor and enhanced PBMC cytokine secretion (IFN-γ and tumour necrosis factor-α) and cytotoxicity. Conclusions IFN-α-induced CD100 on naïve CD8 T cells promotes PBMC cytokine secretion and cytotoxicity through CD100-CD72 signalling during HCV infection.
[Mh] Termos MeSH primário: Antígenos CD/genética
Antígenos de Diferenciação de Linfócitos B/genética
Antivirais/uso terapêutico
Linfócitos T CD8-Positivos/efeitos dos fármacos
Hepatite C/tratamento farmacológico
Interferon-alfa/uso terapêutico
Polietilenoglicóis/uso terapêutico
Semaforinas/genética
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/imunologia
Antígenos de Diferenciação de Linfócitos B/imunologia
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/virologia
Estudos de Casos e Controles
Técnicas de Cocultura
Citotoxicidade Imunológica
Feminino
Regulação da Expressão Gênica
Hepacivirus/efeitos dos fármacos
Hepacivirus/crescimento & desenvolvimento
Hepacivirus/imunologia
Hepatite C/imunologia
Hepatite C/virologia
Seres Humanos
Interferon gama/genética
Interferon gama/imunologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/imunologia
Leucócitos Mononucleares/virologia
Masculino
Meia-Idade
Cultura Primária de Células
RNA Viral/efeitos dos fármacos
Proteínas Recombinantes/uso terapêutico
Semaforinas/imunologia
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (Antiviral Agents); 0 (CD100 antigen); 0 (CD72 protein, human); 0 (Interferon-alpha); 0 (RNA, Viral); 0 (Recombinant Proteins); 0 (Semaphorins); 0 (Tumor Necrosis Factor-alpha); 30IQX730WE (Polyethylene Glycols); 82115-62-6 (Interferon-gamma); Q46947FE7K (peginterferon alfa-2a)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1177/0300060516676136



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