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[PMID]:28460187
[Au] Autor:Li L; Xu G; Duan C
[Ad] Endereço:Department of Burn and Plastic Surgery, Tangshan Gongren Hospital, Tangshan 063000, Hebei, China.
[Ti] Título:TLR2 affects CD86 expression and inflammatory response in burn injury mice through regulation of p38.
[So] Source:Biochem Cell Biol;95(5):549-555, 2017 Oct.
[Is] ISSN:1208-6002
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to assess the effects of TLR2-p38-CD86 signaling pathways on the inflammatory response in a mouse model of burn injury. Wild-type (TLR2 ) and mutant-type (TLR2 ) mice were obtained, and a mouse burn injury model was constructed. Tissue samples were examined with hematoxylin and eosin staining and the transferase mediated nick end labeling (TUNEL) method. Macrophages were treated with TLR2 agonist and p38 inhibitor. The expression levels of TLR2, p38, CD86, IL-1ß, and TNF-α were quantified by RT-qPCR, Western blot, and ELISA. When compared with the sham group, the burn group had a significantly higher rate of apoptosis as well as higher expressions of TLR2, p38, CD86, IL-1ß, and TNF-α. Inhibiting TLR2 was shown to significantly reduce the expressions of p-p38, CD86, IL-1ß, and TNF-α. In the results of in-vitro experiments, TLR2 agonist increased the expression of p-p38, CD86, IL-1ß, and TNF-α, whereas a p38 inhibitor was shown to reduce the expression of CD86, IL-1ß, and TNF-α. Our results suggest that the TLR2-p38-CD86 signaling pathway plays a vital role in inflammation associated with burn injury.
[Mh] Termos MeSH primário: Antígeno B7-2/genética
Queimaduras/metabolismo
Inflamação/metabolismo
Receptor 2 Toll-Like/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/metabolismo
Queimaduras/patologia
Modelos Animais de Doenças
Feminino
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Transdução de Sinais/efeitos dos fármacos
Receptor 2 Toll-Like/agonistas
Receptor 2 Toll-Like/deficiência
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (Cd86 protein, mouse); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1139/bcb-2016-0210


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[PMID]:29262350
[Au] Autor:Suan D; Kräutler NJ; Maag JLV; Butt D; Bourne K; Hermes JR; Avery DT; Young C; Statham A; Elliott M; Dinger ME; Basten A; Tangye SG; Brink R
[Ad] Endereço:Immunology Division, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia; Westmead Clinical School, University of Sydney, Sydney, NSW 2145, Australia.
[Ti] Título:CCR6 Defines Memory B Cell Precursors in Mouse and Human Germinal Centers, Revealing Light-Zone Location and Predominant Low Antigen Affinity.
[So] Source:Immunity;47(6):1142-1153.e4, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC differentiation, no such marker exists for cells committed to the MBC lineage. Here, we report that the chemokine receptor CCR6 uniquely marks MBC precursors in both mouse and human GCs. CCR6 GC B cells were highly enriched within the GC light zone (LZ), were the most quiescent of all GC B cells, exhibited a cell-surface phenotype and gene expression signature indicative of an MBC transition, and possessed the augmented response characteristics of MBCs. MBC precursors within the GC LZ predominantly possessed a low affinity for antigen but also included cells from within the high-affinity pool. These data indicate a fundamental dichotomy between the processes that drive MBC and PC differentiation during GC responses.
[Mh] Termos MeSH primário: Centro Germinativo/imunologia
Imunidade Humoral
Plasmócitos/imunologia
Células Precursoras de Linfócitos B/imunologia
Receptores CCR6/imunologia
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/genética
Antígeno B7-2/imunologia
Diferenciação Celular
Linhagem da Célula/imunologia
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Centro Germinativo/citologia
Seres Humanos
Memória Imunológica
Imunofenotipagem
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Plasmócitos/citologia
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/imunologia
Células Precursoras de Linfócitos B/citologia
Receptores CCR6/genética
Receptores CXCR4/genética
Receptores CXCR4/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (CCR6 protein, mouse); 0 (CXCR4 protein, mouse); 0 (Cd86 protein, mouse); 0 (Prdm1 protein, mouse); 0 (Receptors, CCR6); 0 (Receptors, CXCR4); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28963930
[Au] Autor:Li Y; Yu Q; Zhao W; Zhang J; Liu W; Huang M; Zeng X
[Ad] Endereço:Department of Respiratory & Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu 210029, China.
[Ti] Título:Oligomeric proanthocyanidins attenuate airway inflammation in asthma by inhibiting dendritic cells maturation.
[So] Source:Mol Immunol;91:209-217, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To date, although a promising anti-inflammatory activity of oligomeric proanthocyanidins (OPCs) has been observed in asthma, the mechanism responsible for these immunomodulatory properties remains obscure. Dendritic cells (DCs) that reside in the airway have been widely perceived as an important contributor to asthma. Our study was to demonstrate OPCs' effects on maturation and immunoregulation of pulmonary CD11c dendritic cells (DCs). BALB/c mice were exposed to ovalbumin (OVA) to induce murine model of asthma. In addition, pulmonary DCs and bone marrow-derived DCs (BMDCs) cultures were used to evaluate impacts of OPCs on DCs function. The results obtained here indicated that OPCs treatment dramatically reduced airway inflammation, such as the infiltration of inflammatory cells and the levels of allergen-specific serum IgE and Th2 cytokines. The expression of co-stimulatory molecules especially CD86 distributed on pulmonary DCs and bone marrow-derived DCs (BMDCs) also markedly declined. The phosphorylation of cAMP responsive element-binding protein (CREB) was significantly inhibited while no changes were observed in the expression of cAMP responsive element modulator (CREM). By transferring BMDCs into the airways of naïve mice, we found that OPCs-treated DCs (DC+OVA+OPC) were much less potent in promoting CD4 T cells proliferation than OVA-pulsed DCs (DC+OVA), followed by the ameliorated eosinophilic inflammation in airway. Our findings tailor a novel profile of OPCs in the regulation of DCs function, shedding new light on the therapeutic potential of OPCs in asthma management.
[Mh] Termos MeSH primário: Asma/imunologia
Células Dendríticas/imunologia
Pulmão/imunologia
Proantocianidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Asma/induzido quimicamente
Asma/patologia
Antígeno B7-2/imunologia
Antígeno CD11c/imunologia
Proteína de Ligação a CREB/imunologia
Proliferação Celular/efeitos dos fármacos
Citocinas/imunologia
Células Dendríticas/patologia
Feminino
Imunoglobulina E/imunologia
Inflamação/induzido quimicamente
Inflamação/imunologia
Inflamação/patologia
Pulmão/patologia
Camundongos
Camundongos Endogâmicos BALB C
Fosforilação/efeitos dos fármacos
Fosforilação/imunologia
Células Th2/imunologia
Células Th2/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (CD11c Antigen); 0 (Cd86 protein, mouse); 0 (Cytokines); 0 (Proanthocyanidins); 37341-29-0 (Immunoglobulin E); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, mouse)
[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:171001
[St] Status:MEDLINE


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[PMID]:28822786
[Au] Autor:Chang KT; Lin YL; Lin CT; Hong CJ; Tsai MJ; Huang WC; Shih YH; Lee YY; Cheng H; Huang MC
[Ad] Endereço:Institute of Pharmacology, School of Medicine, National Yang-Ming University, Taipei, Taiwan; Neural Regeneration Laboratory, Department of Neurosurgery, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
[Ti] Título:Leptin is essential for microglial activation and neuropathic pain after preganglionic cervical root avulsion.
[So] Source:Life Sci;187:31-41, 2017 Oct 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Preganglionic cervical root avulsion (PCRA) affects both the peripheral and central nervous systems and is often associated with neuropathic pain. Unlike peripheral nerve injuries (PNI), central lesions caused by disruption of cervical roots from the spinal cord following PCRA contribute to the generation of neuropathic pain. Leptin is involved in the development of neuropathic pain after PNI by affecting neurons. However, whether leptin is involved in microglial activation leading to neuropathic pain after PCRA is unknown. MAIN METHODS: Preganglionic avulsion of the left 6 -8 cervical roots was performed in C57B/6J mice and leptin-deficient mice. A leptin antagonist or leptin was administered to C57B/6J mice and leptin-deficient mice after injury, respectively. The expression pattern of spinal and supraspinal microglia was examined by immunofluorescent staining. Von Frey filaments were used to test pain sensitivity. KEY FINDINGS: Leptin is essential for the development of neuropathic pain after PCRA. Allodynia was absent in the leptin-deficient mice and the mice administered the leptin antagonist. We also found that leptin deficiency or the administration of its antagonist inhibited the development of microgliosis in the dorsal horn and brainstem. Furthermore, increase in the expression of CD86 and iNOS, and Wallerian degeneration were noted in the spinal cord. The administration of exogenous leptin to leptin-deficient mice reversed these effects. SIGNIFICANCE: We concluded that leptin is involved in the proliferation and activation of microglia, which in turn enhances the development of neuropathic pain. Blocking the effects of leptin might be a target for the treatment of neuropathic pain after PCRA.
[Mh] Termos MeSH primário: Fratura Avulsão/fisiopatologia
Leptina/fisiologia
Microglia/fisiologia
Neuralgia/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/biossíntese
Tronco Encefálico/efeitos dos fármacos
Tronco Encefálico/patologia
Proliferação Celular/fisiologia
Medula Cervical/lesões
Feminino
Fratura Avulsão/complicações
Fratura Avulsão/patologia
Gliose/prevenção & controle
Leptina/antagonistas & inibidores
Leptina/genética
Leptina/farmacologia
Masculino
Camundongos
Camundongos Transgênicos
Microglia/efeitos dos fármacos
Neuralgia/complicações
Óxido Nítrico Sintase Tipo II/biossíntese
Medição da Dor/efeitos dos fármacos
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
Medula Espinal/patologia
Corno Dorsal da Medula Espinal/efeitos dos fármacos
Corno Dorsal da Medula Espinal/patologia
Degeneração Walleriana/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (Leptin); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse)
[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:170821
[St] Status:MEDLINE


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[PMID]:28719732
[Au] Autor:McIntosh LA; Marion MC; Sudman M; Comeau ME; Becker ML; Bohnsack JF; Fingerlin TE; Griffin TA; Haas JP; Lovell DJ; Maier LA; Nigrovic PA; Prahalad S; Punaro M; Rosé CD; Wallace CA; Wise CA; Moncrieffe H; Howard TD; Langefeld CD; Thompson SD
[Ad] Endereço:Cincinnati Children's Hospital Medical Center and University of Cincinnati, Cincinnati, Ohio.
[Ti] Título:Genome-Wide Association Meta-Analysis Reveals Novel Juvenile Idiopathic Arthritis Susceptibility Loci.
[So] Source:Arthritis Rheumatol;69(11):2222-2232, 2017 Nov.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Juvenile idiopathic arthritis (JIA) is the most common childhood rheumatic disease and has a strong genomic component. To date, JIA genetic association studies have had limited sample sizes, used heterogeneous patient populations, or included only candidate regions. The aim of this study was to identify new associations between JIA patients with oligoarticular disease and those with IgM rheumatoid factor (RF)-negative polyarticular disease, which are clinically similar and the most prevalent JIA disease subtypes. METHODS: Three cohorts comprising 2,751 patients with oligoarticular or RF-negative polyarticular JIA were genotyped using the Affymetrix Genome-Wide SNP Array 6.0 or the Illumina HumanCoreExome-12+ Array. Overall, 15,886 local and out-of-study controls, typed on these platforms or the Illumina HumanOmni2.5, were used for association analyses. High-quality single-nucleotide polymorphisms (SNPs) were used for imputation to 1000 Genomes prior to SNP association analysis. RESULTS: Meta-analysis showed evidence of association (P < 1 × 10 ) at 9 regions: PRR9_LOR (P = 5.12 × 10 ), ILDR1_CD86 (P = 6.73 × 10 ), WDFY4 (P = 1.79 × 10 ), PTH1R (P = 1.87 × 10 ), RNF215 (P = 3.09 × 10 ), AHI1_LINC00271 (P = 3.48 × 10 ), JAK1 (P = 4.18 × 10 ), LINC00951 (P = 5.80 × 10 ), and HBP1 (P = 7.29 × 10 ). Of these, PRR9_LOR, ILDR1_CD86, RNF215, LINC00951, and HBP1 were shown, for the first time, to be autoimmune disease susceptibility loci. Furthermore, associated SNPs included cis expression quantitative trait loci for WDFY4, CCDC12, MTP18, SF3A1, AHI1, COG5, HBP1, and GPR22. CONCLUSION: This study provides evidence of both unique JIA risk loci and risk loci overlapping between JIA and other autoimmune diseases. These newly associated SNPs are shown to influence gene expression, and their bounding regions tie into molecular pathways of immunologic relevance. Thus, they likely represent regions that contribute to the pathology of oligoarticular JIA and RF-negative polyarticular JIA.
[Mh] Termos MeSH primário: Artrite Juvenil/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transporte Vesicular/genética
Antígeno B7-2/genética
Criança
Pré-Escolar
Feminino
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Proteínas de Grupo de Alta Mobilidade/genética
Seres Humanos
Lactente
Peptídeos e Proteínas de Sinalização Intracelular/genética
Janus Quinase 1/genética
Masculino
Proteínas Mitocondriais/genética
Polimorfismo de Nucleotídeo Único
Proteínas/genética
Locos de Características Quantitativas/genética
Fatores de Processamento de RNA/genética
Receptor Tipo 1 de Hormônio Paratireóideo/genética
Receptores de Superfície Celular/genética
Receptores Acoplados a Proteínas-G/genética
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (AHI1 protein, human); 0 (Adaptor Proteins, Signal Transducing); 0 (Adaptor Proteins, Vesicular Transport); 0 (B7-2 Antigen); 0 (CCDC12 protein, human); 0 (COG5 protein, human); 0 (GPR22 protein, human); 0 (HBP1 protein, human); 0 (High Mobility Group Proteins); 0 (ILDR1 protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (MTP18 protein, human); 0 (Mitochondrial Proteins); 0 (PTH1R protein, human); 0 (Proteins); 0 (RNA Splicing Factors); 0 (Receptor, Parathyroid Hormone, Type 1); 0 (Receptors, Cell Surface); 0 (Receptors, G-Protein-Coupled); 0 (Repressor Proteins); 0 (SF3A1 protein, human); 0 (WDFY4 protein, human); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (Janus Kinase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1002/art.40216


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[PMID]:28715682
[Au] Autor:Kraaij MD; van Dijk A; Haagsman HP
[Ad] Endereço:Division of Molecular Host Defence, Dept. of Infectious Diseases & Immunology, Utrecht University, Utrecht, The Netherlands.
[Ti] Título:CATH-2 and LL-37 increase mannose receptor expression, antigen presentation and the endocytic capacity of chicken mononuclear phagocytes.
[So] Source:Mol Immunol;90:118-125, 2017 Oct.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cathelicidins display in vitro and in vivo immunomodulatory activities and are part of the innate immune system. Previously, we found that in ovo treatment with chicken cathelicidin CATH-2 partially protects young broilers against respiratory E. coli infection. To determine the cellular aspects of this protection, we investigated immunomodulatory effects of CATH-2 and the human cathelicidin LL-37 on primary chicken peripheral blood mononuclear cells (PBMCs). Treatment of chicken PBMCs with L-CATH-2, D-CATH-2 or LL-37 increased the percentage of mononuclear phagocytes, but decreased that of B cells. L-CATH-2, D-CATH-2 and LL-37 treatment of chicken PBMCs also enhanced the expression levels of mannose receptor MRC1 and antigen presentation markers MHCII, CD40 and CD86 on mononuclear phagocytes, indicating increased antigen presentation capacity. Concomitantly, L-CATH-2, D-CATH-2 and LL-37 neutralized LPS-induced cytokine production, while increasing the endocytic capacity. We conclude that L-CATH-2, D-CATH-2 and LL-37 can modulate the immune response of primary chicken immune cells by increasing mannose receptor expression, antigen presentation, endocytosis and neutralizing LPS-induced cytokine production and as a result augment activation of the adaptive immune system.
[Mh] Termos MeSH primário: Apresentação do Antígeno/imunologia
Peptídeos Catiônicos Antimicrobianos/imunologia
Endocitose/imunologia
Lectinas Tipo C/biossíntese
Lectinas de Ligação a Manose/biossíntese
Receptores de Superfície Celular/biossíntese
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/metabolismo
Antígenos CD40/metabolismo
Proliferação Celular
Células Cultivadas
Galinhas
Citocinas/biossíntese
Seres Humanos
Lectinas Tipo C/imunologia
Lectinas de Ligação a Manose/imunologia
Sistema Fagocitário Mononuclear/imunologia
Receptores de Superfície Celular/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (B7-2 Antigen); 0 (CD40 Antigens); 0 (CMAP27 protein, chicken); 0 (Cytokines); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, Cell Surface); 0 (mannose receptor); 143108-26-3 (CAP18 lipopolysaccharide-binding protein)
[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:170718
[St] Status:MEDLINE


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[PMID]:28688767
[Au] Autor:Na-Ek P; Thewsoongnoen J; Thanunchai M; Wiboon-Ut S; Sa-Ard-Iam N; Mahanonda R; Thitithanyanont A
[Ad] Endereço:Department of Microbiology, Faculty of Science, Mahidol University, Bangkok, Thailand.
[Ti] Título:The activation of B cells enhances DC-SIGN expression and promotes susceptibility of B cells to HPAI H5N1 infection.
[So] Source:Biochem Biophys Res Commun;490(4):1301-1306, 2017 Sep 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interplay between highly pathogenic avian influenza (HPAI) H5N1 virus and immune cells has been extensively studied for years, as host immune components are thought to play significant roles in promoting the systemic spread of the virus and responsible for cytokine storm. Previous studies suggested that the interaction of B cells and monocytes could promote HPAI H5N1 infection by enhancing avian influenza virus receptor expression. In this study, we further investigate the relationship between the HPAI H5N1 virus, activated B cells, and DC-SIGN expression. DC-SIGN has been described as an important factor for mediating various types of viral infection. Here, we first demonstrate that HPAI H5N1 infection could induce an activation of B cells, which was associated with DC-SIGN expression. Using CD40L and recombinant IL-4 for B cell stimulation, we determined that DC-SIGN expressed on activated B cells was able to enhance its susceptibility to HPAI H5N1 infection. Our findings uncover the interplay between this H5N1 virus and B cells and provide important information in understanding how the virus overcomes our immune system, contributing to its unusual immunopathogenesis.
[Mh] Termos MeSH primário: Linfócitos B/virologia
Moléculas de Adesão Celular/imunologia
Interações Hospedeiro-Patógeno
Vírus da Influenza A Subtipo H5N1/fisiologia
Lectinas Tipo C/imunologia
Receptores de Superfície Celular/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Antígeno B7-2/genética
Antígeno B7-2/imunologia
Aves/virologia
Ligante de CD40/farmacologia
Moléculas de Adesão Celular/genética
Suscetibilidade a Doenças
Regulação da Expressão Gênica
Seres Humanos
Vírus da Influenza A Subtipo H5N1/isolamento & purificação
Interleucina-4/farmacologia
Lectinas Tipo C/genética
Ativação Linfocitária/efeitos dos fármacos
Cultura Primária de Células
Receptores de Superfície Celular/genética
Proteínas Recombinantes/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (CD86 protein, human); 0 (Cell Adhesion Molecules); 0 (DC-specific ICAM-3 grabbing nonintegrin); 0 (IL4 protein, human); 0 (Lectins, C-Type); 0 (Receptors, Cell Surface); 0 (Recombinant Proteins); 147205-72-9 (CD40 Ligand); 207137-56-2 (Interleukin-4)
[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:170710
[St] Status:MEDLINE


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[PMID]:28631301
[Au] Autor:Laurent L; Le Fur A; Bloas RL; Néel M; Mary C; Moreau A; Poirier N; Vanhove B; Fakhouri F
[Ad] Endereço:INSERM UMR 1064, Nantes, France.
[Ti] Título:Prevention of lupus nephritis development in NZB/NZW mice by selective blockade of CD28.
[So] Source:Eur J Immunol;47(8):1368-1376, 2017 Aug.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Systemic lupus erythematosus (SLE) is a chronic systemic inflammatory disease. Autoantibodies (autoAbs) against double-stranded DNA (ds DNA), the hallmark of lupus, are produced and maintained by the interaction between auto-reactive B cells and CD4 T cells. This interplay is controlled by the CD28/CD80-86/CTLA-4 axis. Here we investigated whether selective blockade of CD28-CD80/86 co-stimulatory interactions abrogates lupus nephritis development in a murine model of SLE. To this aim, NZB/NZW F1 mice were treated for 3 months, either with an anti-CD28 Fab' fragment or a control Fab'-IgG. The effect of CD28 blockade on lupus nephritis onset, survival, production of anti-ds DNA antibodies and costimulatory molecules was evaluated. CD28 blockade prevented the development of lupus nephritis and prolonged survival during the 3-month treatment and 12 weeks after. Furthermore, the production of anti-ds DNA autoAbs was decreased. Lastly, the protective effect of CD28 blockade was associated with increased intrarenal expression of the immunoregulatory molecule, Indoleamine 2, 3-dioxygenase, of the co-inhibitory receptor programmed cell-Death - 1 (PD-1) and of its ligand programmed death ligand - 1 (PDL-1).In conclusion, CD28 blockade prevented the development of lupus nephritis in NZB/NZW F1 mice. This immunomodulatory strategy is a promising candidate for SLE therapy in humans.
[Mh] Termos MeSH primário: Anticorpos Antinucleares/sangue
Autoanticorpos/sangue
Antígenos CD28/antagonistas & inibidores
Imunoterapia/métodos
Nefrite Lúpica/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anticorpos Antinucleares/imunologia
Autoanticorpos/imunologia
Linfócitos B/imunologia
Antígeno B7-1/antagonistas & inibidores
Antígeno B7-1/imunologia
Antígeno B7-1/metabolismo
Antígeno B7-2/antagonistas & inibidores
Antígeno B7-2/imunologia
Antígeno B7-2/metabolismo
Antígenos CD28/imunologia
Linfócitos T CD4-Positivos/imunologia
Modelos Animais de Doenças
Feminino
Fragmentos Fab das Imunoglobulinas/administração & dosagem
Indolamina-Pirrol 2,3,-Dioxigenase/genética
Indolamina-Pirrol 2,3,-Dioxigenase/imunologia
Rim/imunologia
Rim/patologia
Lúpus Eritematoso Sistêmico/imunologia
Nefrite Lúpica/imunologia
Camundongos
Camundongos Endogâmicos NZB
Receptor de Morte Celular Programada 1/genética
Receptor de Morte Celular Programada 1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Autoantibodies); 0 (B7-1 Antigen); 0 (B7-2 Antigen); 0 (CD28 Antigens); 0 (Cd86 protein, mouse); 0 (Immunoglobulin Fab Fragments); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Pdcd1 protein, mouse); 0 (Programmed Cell Death 1 Receptor)
[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:170621
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201746923


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[PMID]:28628673
[Au] Autor:Chang NH; Manion KP; Loh C; Pau E; Baglaenko Y; Wither JE
[Ad] Endereço:Arthritis Centre of Excellence, Division of Genetics and Development, Krembil Research Institute, Toronto, Ontario, Canada.
[Ti] Título:Multiple tolerance defects contribute to the breach of B cell tolerance in New Zealand Black chromosome 1 congenic mice.
[So] Source:PLoS One;12(6):e0179506, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lupus is characterized by a loss of B cell tolerance leading to autoantibody production. In this study, we explored the mechanisms underlying this loss of tolerance using B6 congenic mice with an interval from New Zealand Black chromosome 1 (denoted c1(96-100)) sufficient for anti-nuclear antibody production. Transgenes for soluble hen egg white lysozyme (sHEL) and anti-HEL immunoglobulin were crossed onto this background and various tolerance mechanisms examined. We found that c1(96-100) mice produced increased levels of IgM and IgG anti-HEL antibodies compared to B6 mice and had higher proportions of germinal center B cells and long-lived plasma cells, suggesting a germinal center-dependent breach of B cell anergy. Consistent with impaired anergy induction, c1(96-100) double transgenic B cells showed enhanced survival and CD86 upregulation. Hematopoietic chimeric sHEL mice with a mixture of B6 and c1(96-100) HEL transgenic B cells recapitulated these results, suggesting the presence of a B cell autonomous defect. Surprisingly, however, there was equivalent recruitment of B6 and c1(96-100) B cells into germinal centers and differentiation to splenic plasmablasts in these mice. In contrast, there were increased proportions of c1(96-100) T follicular helper cells and long-lived plasma cells as compared to their B6 counterparts, suggesting that both B and T cell defects are required to breach germinal center tolerance in this model. This possibility was further supported by experiments showing an enhanced breach of anergy in double transgenic mice with a longer chromosome 1 interval with additional T cell defects.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Cromossomos/genética
Tolerância Imunológica
[Mh] Termos MeSH secundário: Animais
Apoptose
Linfócitos B/citologia
Linfócitos B/imunologia
Antígeno B7-2/metabolismo
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/metabolismo
Diferenciação Celular
Galinhas
Cromossomos/metabolismo
Imunoglobulinas/genética
Imunoglobulinas/metabolismo
Camundongos
Camundongos Congênicos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microscopia de Fluorescência
Muramidase/genética
Muramidase/metabolismo
Nova Zelândia
Fosfatidilinositol 3-Quinases/metabolismo
Baço/metabolismo
Baço/patologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (Immunoglobulins); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.2.1.- (hen egg lysozyme); EC 3.2.1.17 (Muramidase)
[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:170620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179506


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[PMID]:28586386
[Au] Autor:Clemente AM; Castronovo G; Antonelli A; D'Andrea MM; Tanturli M; Perissi E; Paccosi S; Parenti A; Cozzolino F; Rossolini GM; Torcia MG
[Ad] Endereço:Department of Experimental and Clinical Medicine, University of Firenze, Firenze, Italy.
[Ti] Título:Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC-type carbapenemase.
[So] Source:PLoS One;12(6):e0178847, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsiella pneumoniae (KP) strains belonging to the clonal group (CG) 258, including sequence type (ST) 258 and other related STs. Two distinct clades of CG258-KP have evolved, which differ mainly for the composition of their capsular polysaccharides, and recent studies indicate that clade 1 evolved from an ancestor of clade 2 by recombination of a genomic fragment carrying the capsular polysaccharide (cps) locus. In this paper, we investigated the ability of two ST258-KP strains, KKBO-1 and KK207-1, selected as representatives of ST258-KP clade 2 and clade 1, respectively, to activate an adaptive immune response using ex vivo-stimulation of PBMC from normal donors as an experimental model. Our data showed that KKBO-1 (clade 2) induces a Th17 response more efficiently than KK207-1 (clade 1): the percentage of CD4+IL17+ cells and the production of IL-17A were significantly higher in cultures with KKBO-1 compared to cultures with KK207-1. While no differences in the rate of bacterial internalization or in the bacteria-induced expression of CD86 and HLA-DR by monocytes and myeloid dendritic cells were revealed, we found that the two strains significantly differ in inducing the production of cytokines involved in the adaptive immune response, as IL-1ß, IL-23 and TNF-α, by antigen-presenting cells, with KKBO-1 being a more efficient inducer than KK207-1. The immune responses elicited by KK207-1 were comparable to those elicited by CIP 52.145, a highly virulent K. pneumoniae reference strain known to escape immune-inflammatory responses. Altogether, present results suggest that CG258-KP of the two clades are capable of inducing a different response of adaptive immunity in the human host.
[Mh] Termos MeSH primário: Imunidade Adaptativa/imunologia
Proteínas de Bactérias/imunologia
Interações Hospedeiro-Patógeno/imunologia
Infecções por Klebsiella/imunologia
Klebsiella pneumoniae/imunologia
beta-Lactamases/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/genética
Células Apresentadoras de Antígenos/imunologia
Antígeno B7-2/imunologia
Proteínas de Bactérias/biossíntese
Linfócitos T CD4-Positivos/imunologia
Células Dendríticas/imunologia
Genoma Bacteriano
Antígenos HLA-DR/imunologia
Seres Humanos
Interleucina-17/imunologia
Infecções por Klebsiella/genética
Infecções por Klebsiella/patologia
Klebsiella pneumoniae/patogenicidade
Filogenia
Células Th17/imunologia
Fator de Necrose Tumoral alfa/imunologia
beta-Lactamases/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (Bacterial Proteins); 0 (HLA-DR Antigens); 0 (Interleukin-17); 0 (Tumor Necrosis Factor-alpha); EC 3.5.2.6 (beta-Lactamases); EC 3.5.2.6 (carbapenemase)
[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:170607
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178847



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