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  1 / 3428 MEDLINE  
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[PMID]:28978694
[Au] Autor:Catalan-Dibene J; Vazquez MI; Luu VP; Nuccio SP; Karimzadeh A; Kastenschmidt JM; Villalta SA; Ushach I; Pone EJ; Casali P; Raffatellu M; Burkhardt AM; Hernandez-Ruiz M; Heller G; Hevezi PA; Zlotnik A
[Ad] Endereço:Department of Physiology and Biophysics, University of California, Irvine, Irvine, CA 92697.
[Ti] Título:Identification of IL-40, a Novel B Cell-Associated Cytokine.
[So] Source:J Immunol;199(9):3326-3335, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We describe a novel B cell-associated cytokine, encoded by an uncharacterized gene ( ; chromosome 17 open reading frame 99), that is expressed in bone marrow and fetal liver and whose expression is also induced in peripheral B cells upon activation. is only present in mammalian genomes, and it encodes a small (∼27-kDa) secreted protein unrelated to other cytokine families, suggesting a function in mammalian immune responses. Accordingly, expression is induced in the mammary gland upon the onset of lactation, and a mouse exhibits reduced levels of IgA in the serum, gut, feces, and lactating mammary gland. mice have smaller and fewer Peyer's patches and lower numbers of IgA-secreting cells. The microbiome of mice exhibits altered composition, likely a consequence of the reduced levels of IgA in the gut. Although naive B cells can express upon activation, their production increases following culture with various cytokines, including IL-4 and TGF-ß1, suggesting that differentiation can result in the expansion of -producing B cells during some immune responses. Taken together, these observations indicate that encodes a novel B cell-associated cytokine, which we have called IL-40, that plays an important role in humoral immune responses and may also play a role in B cell development. Importantly, IL-40 is also expressed by human activated B cells and by several human B cell lymphomas. The latter observations suggest that it may play a role in the pathogenesis of certain human diseases.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Regulação da Expressão Gênica/imunologia
Interleucinas/imunologia
Nódulos Linfáticos Agregados/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Imunoglobulina A/imunologia
Interleucinas/genética
Células Jurkat
Linfoma de Células B/genética
Linfoma de Células B/imunologia
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin A); 0 (Interleukins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171104
[Lr] Data última revisão:
171104
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700534


  2 / 3428 MEDLINE  
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[PMID]:28972089
[Au] Autor:Bednar KJ; Shanina E; Ballet R; Connors EP; Duan S; Juan J; Arlian BM; Kulis MD; Butcher EC; Fung-Leung WP; Rao TS; Paulson JC; Macauley MS
[Ad] Endereço:Immunology Team, Janssen Research and Development, LLC, Raritan, NJ 08869.
[Ti] Título:Human CD22 Inhibits Murine B Cell Receptor Activation in a Human CD22 Transgenic Mouse Model.
[So] Source:J Immunol;199(9):3116-3128, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD22, a sialic acid-binding Ig-type lectin (Siglec) family member, is an inhibitory coreceptor of the BCR with established roles in health and disease. The restricted expression pattern of CD22 on B cells and most B cell lymphomas has made CD22 a therapeutic target for B cell-mediated diseases. Models to better understand how in vivo targeting of CD22 translates to human disease are needed. In this article, we report the development of a transgenic mouse expressing human CD22 (hCD22) in B cells and assess its ability to functionally substitute for murine CD22 (mCD22) for regulation of BCR signaling, Ab responses, homing, and tolerance. Expression of hCD22 on transgenic murine B cells is comparable to expression on human primary B cells, and it colocalizes with mCD22 on the cell surface. Murine B cells expressing only hCD22 have identical calcium (Ca ) flux responses to anti-IgM as mCD22-expressing wild-type B cells. Furthermore, hCD22 transgenic mice on an mCD22 background have restored levels of marginal zone B cells and Ab responses compared with deficiencies observed in CD22 mice. Consistent with these observations, hCD22 transgenic mice develop normal humoral responses in a peanut allergy oral sensitization model. Homing of B cells to Peyer's patches was partially rescued by expression of hCD22 compared with CD22 B cells, although not to wild-type levels. Notably, Siglec-engaging antigenic liposomes formulated with an hCD22 ligand were shown to prevent B cell activation, increase cell death, and induce tolerance in vivo. This hCD22 transgenic mouse will be a valuable model for investigating the function of hCD22 and preclinical studies targeting hCD22.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Hipersensibilidade a Amendoim/imunologia
Nódulos Linfáticos Agregados/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/patologia
Modelos Animais de Doenças
Seres Humanos
Ativação Linfocitária/genética
Camundongos
Camundongos Transgênicos
Hipersensibilidade a Amendoim/genética
Hipersensibilidade a Amendoim/patologia
Nódulos Linfáticos Agregados/patologia
Receptores de Antígenos de Linfócitos B/genética
Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD22 protein, human); 0 (Cd22 protein, mouse); 0 (Receptors, Antigen, B-Cell); 0 (Sialic Acid Binding Ig-like Lectin 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700898


  3 / 3428 MEDLINE  
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[PMID]:28898292
[Au] Autor:Elderman M; Sovran B; Hugenholtz F; Graversen K; Huijskes M; Houtsma E; Belzer C; Boekschoten M; de Vos P; Dekker J; Wells J; Faas M
[Ad] Endereço:Top Institute Food and Nutrition, Wageningen, the Netherlands.
[Ti] Título:The effect of age on the intestinal mucus thickness, microbiota composition and immunity in relation to sex in mice.
[So] Source:PLoS One;12(9):e0184274, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A mucus layer covers and protects the intestinal epithelial cells from direct contact with microbes. This mucus layer not only prevents inflammation but also plays an essential role in microbiota colonization, indicating the complex interplay between mucus composition-microbiota and intestinal health. However, it is unknown whether the mucus layer is influenced by age or sex and whether this contributes to reported differences in intestinal diseases in males and females or with ageing. Therefore, in this study we investigated the effect of age on mucus thickness, intestinal microbiota composition and immune composition in relation to sex. The ageing induced shrinkage of the colonic mucus layer was associated with bacterial penetration and direct contact of bacteria with the epithelium in both sexes. Additionally, several genes involved in the biosynthesis of mucus were downregulated in old mice, especially in males, and this was accompanied by a decrease in abundances of various Lactobacillus species and unclassified Clostridiales type IV and XIV and increase in abundance of the potential pathobiont Bacteroides vulgatus. The changes in mucus and microbiota in old mice were associated with enhanced activation of the immune system as illustrated by a higher percentage of effector T cells in old mice. Our data contribute to a better understanding of the interplay between mucus-microbiota-and immune responses and ultimately may lead to more tailored design of strategies to modulate mucus production in targeted groups.
[Mh] Termos MeSH primário: Microbioma Gastrointestinal/imunologia
Imunidade nas Mucosas
Mucosa Intestinal/citologia
Mucosa Intestinal/imunologia
[Mh] Termos MeSH secundário: Fatores Etários
Envelhecimento/imunologia
Envelhecimento/metabolismo
Animais
Biodiversidade
Diferenciação Celular/genética
Diferenciação Celular/imunologia
Colo/citologia
Colo/imunologia
Colo/metabolismo
Colo/microbiologia
Células Dendríticas/citologia
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Feminino
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Mucosa Intestinal/metabolismo
Masculino
Metagenoma
Metagenômica/métodos
Camundongos
Muco/metabolismo
Nódulos Linfáticos Agregados/imunologia
Nódulos Linfáticos Agregados/metabolismo
Fatores Sexuais
Transdução de Sinais
Baço/imunologia
Baço/metabolismo
Linfócitos T/citologia
Linfócitos T/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184274


  4 / 3428 MEDLINE  
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[PMID]:28846085
[Au] Autor:He Z; Ma J; Wang R; Zhang J; Huang Z; Wang F; Sen S; Rothenberg EV; Sun Z
[Ad] Endereço:Division of Molecular Immunology, Beckman Research Institute of City of Hope, Duarte, California, USA.
[Ti] Título:A two-amino-acid substitution in the transcription factor RORγt disrupts its function in T 17 differentiation but not in thymocyte development.
[So] Source:Nat Immunol;18(10):1128-1138, 2017 Oct.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor RORγt regulates differentiation of the T 17 subset of helper T cells, thymic T cell development and lymph-node genesis. Although elimination of RORγt prevents T 17 cell-mediated experimental autoimmune encephalomyelitis (EAE), it also disrupts thymocyte development, which could lead to lethal thymic lymphoma. Here we identified a two-amino-acid substitution in RORγt (RORγt ) that 'preferentially' disrupted T 17 differentiation but not thymocyte development. Mice expressing RORγt were resistant to EAE associated with defective T 17 differentiation but maintained normal thymocyte development and normal lymph-node genesis, except for Peyer's patches. RORγt showed less ubiquitination at Lys69 that was selectively required for T 17 differentiation but not T cell development. This study will inform the development of treatments that selectively target T 17 cell-mediated autoimmunity but do not affect thymocyte development or induce lymphoma.
[Mh] Termos MeSH primário: Substituição de Aminoácidos
Diferenciação Celular/genética
Mutação
Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/genética
Células Th17/citologia
Células Th17/metabolismo
Timócitos/citologia
Timócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Diferenciação Celular/imunologia
Análise por Conglomerados
Encefalomielite Autoimune Experimental/genética
Encefalomielite Autoimune Experimental/imunologia
Encefalomielite Autoimune Experimental/metabolismo
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Imunofenotipagem
Linfonodos/imunologia
Linfonodos/metabolismo
Camundongos
Camundongos Knockout
Nódulos Linfáticos Agregados/imunologia
Nódulos Linfáticos Agregados/metabolismo
Subpopulações de Linfócitos T/citologia
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Células Th17/imunologia
Timócitos/imunologia
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Nuclear Receptor Subfamily 1, Group F, Member 3)
[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:170829
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3832


  5 / 3428 MEDLINE  
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[PMID]:28716827
[Au] Autor:Davicino RC; Méndez-Huergo SP; Eliçabe RJ; Stupirski JC; Autenrieth I; Di Genaro MS; Rabinovich GA
[Ad] Endereço:División de Inmunología, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis e Instituto Multidisciplinario de Investigaciones Biológicas, Consejo Nacional de Investigaciones Científicas y Técnicas, C5700 San Luis, Argentina.
[Ti] Título:Galectin-1-Driven Tolerogenic Programs Aggravate Infection by Repressing Antibacterial Immunity.
[So] Source:J Immunol;199(4):1382-1392, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:is an enteropathogenic bacterium that causes gastrointestinal disorders, as well as extraintestinal manifestations. To subvert the host's immune response, uses a type III secretion system consisting of an injectisome and effector proteins, called outer proteins (Yops), that modulate activation, signaling, and survival of immune cells. In this article, we show that galectin-1 (Gal-1), an immunoregulatory lectin widely expressed in mucosal tissues, contributes to pathogenicity by undermining protective antibacterial responses. We found higher expression of Gal-1 in the spleen and Peyer's patches of mice infected orogastrically with serotype O:8 compared with noninfected hosts. This effect was prevented when mice were infected with lacking YopP or YopH, two critical effectors involved in bacterial immune evasion. Consistent with a regulatory role for this lectin during pathogenesis, mice lacking Gal-1 showed increased weight and survival, lower bacterial load, and attenuated intestinal pathology compared with wild-type mice. These protective effects involved modulation of NF-κB activation, TNF production, and NO synthesis in mucosal tissue and macrophages, as well as systemic dysregulation of IL-17 and IFN-γ responses. In vivo neutralization of these proinflammatory cytokines impaired bacterial clearance and eliminated host protection conferred by Gal-1 deficiency. Finally, supplementation of recombinant Gal-1 in mice lacking Gal-1 or treatment of wild-type mice with a neutralizing anti-Gal-1 mAb confirmed the immune inhibitory role of this endogenous lectin during infection. Thus, targeting Gal-1-glycan interactions may contribute to reinforce antibacterial responses by reprogramming innate and adaptive immune mechanisms.
[Mh] Termos MeSH primário: Galectina 1/metabolismo
Interações Hospedeiro-Patógeno
Yersiniose/imunologia
Yersinia enterocolitica/imunologia
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Proteínas da Membrana Bacteriana Externa/genética
Proteínas de Bactérias/genética
Galectina 1/antagonistas & inibidores
Galectina 1/genética
Galectina 1/imunologia
Interferon gama/sangue
Interferon gama/imunologia
Interleucina-17/sangue
Interleucina-17/imunologia
Intestinos/imunologia
Intestinos/microbiologia
Intestinos/patologia
Camundongos
NF-kappa B/metabolismo
Óxido Nítrico/biossíntese
Nódulos Linfáticos Agregados/imunologia
Nódulos Linfáticos Agregados/microbiologia
Nódulos Linfáticos Agregados/patologia
Proteínas Tirosina Fosfatases/deficiência
Proteínas Tirosina Fosfatases/genética
Baço/imunologia
Baço/microbiologia
Fator de Necrose Tumoral alfa/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Outer Membrane Proteins); 0 (Bacterial Proteins); 0 (Galectin 1); 0 (Interleukin-17); 0 (NF-kappa B); 0 (Tumor Necrosis Factor-alpha); 0 (YopP protein, Yersinia); 31C4KY9ESH (Nitric Oxide); 82115-62-6 (Interferon-gamma); EC 3.1.3.48 (Protein Tyrosine Phosphatases); EC 3.1.3.48 (yopH protein, Yersinia)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700579


  6 / 3428 MEDLINE  
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[PMID]:28654161
[Au] Autor:Wilmore JR; Jones DD; Allman D
[Ad] Endereço:The Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA.
[Ti] Título:Protocol for improved resolution of plasma cell subpopulations by flow cytometry.
[So] Source:Eur J Immunol;47(8):1386-1388, 2017 Aug.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Plasma cells are rare cells that have been notoriously difficult to detect by flow cytometry. New advances have described B220+ CD138+ plasma cells in the bone marrow that are particularly difficult to distinguish between CD138 intermediate B220+ developing B cells. Herein we describe a novel method for detecting plasma cells in the bone marrow using a combination of CD138 and Sca-1 staining.
[Mh] Termos MeSH primário: Antígenos Ly/análise
Citometria de Fluxo/métodos
Imunofenotipagem/métodos
Proteínas de Membrana/análise
Plasmócitos/classificação
Plasmócitos/imunologia
Sindecana-1/análise
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/imunologia
Antígenos Comuns de Leucócito/análise
Camundongos
Nódulos Linfáticos Agregados/citologia
Nódulos Linfáticos Agregados/imunologia
Fator 1 de Ligação ao Domínio I Regulador Positivo
Baço/citologia
Baço/imunologia
Fatores de Transcrição/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Ly6a protein, mouse); 0 (Membrane Proteins); 0 (Prdm1 protein, mouse); 0 (Sdc1 protein, mouse); 0 (Syndecan-1); 0 (Transcription Factors); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1); EC 3.1.3.48 (Leukocyte Common Antigens)
[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:170628
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201746944


  7 / 3428 MEDLINE  
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[PMID]:28617450
[Au] Autor:Beloqui A; Brayden DJ; Artursson P; Préat V; des Rieux A
[Ad] Endereço:Department of Advanced Drug Delivery and Biomaterials, Louvain Drug Research Institute, Université catholique de Louvain, Brussels, Belgium.
[Ti] Título:A human intestinal M-cell-like model for investigating particle, antigen and microorganism translocation.
[So] Source:Nat Protoc;12(7):1387-1399, 2017 Jul.
[Is] ISSN:1750-2799
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The specialized microfold cells (M cells) in the follicle-associated epithelium (FAE) of intestinal Peyer's patches serve as antigen-sampling cells of the intestinal innate immune system. Unlike 'classical' enterocytes, they are able to translocate diverse particulates without digesting them. They act as pathways for microorganism invasion and mediate food tolerance by transcellular transport of intestinal microbiota and antigens. Their ability to transcytose intact particles can be used to develop oral drug delivery and oral immunization strategies. This protocol describes a reproducible and versatile human M-cell-like in vitro model. This model can be exploited to evaluate M-cell transport of microparticles and nanoparticles for protein, drug or vaccine delivery and to study bacterial adherence and translocation across M cells. The inverted in vitro M-cell model consists of three main steps. First, Caco-2 cells are seeded at the apical side of the inserts. Second, the inserts are inverted and B lymphocytes are seeded at the basolateral side of the inserts. Third, the conversion to M cells is assessed. Although various M-cell culture systems exist, this model provides several advantages over the rest: (i) it is based on coculture with well-established differentiated human cell lines; (ii) it is reproducible under the conditions described herein; (iii) it can be easily mastered; and (iv) it does not require the isolation of primary cells or the use of animals. The protocol requires skills in cell culture and microscopy analysis. The model is obtained after 3 weeks, and transport experiments across the differentiated model can be carried out over periods of up to 10 h.
[Mh] Termos MeSH primário: Antígenos/metabolismo
Técnicas Citológicas/métodos
Células Epiteliais/fisiologia
Material Particulado/metabolismo
Nódulos Linfáticos Agregados/citologia
Transcitose
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Particulate Matter)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1038/nprot.2017.041


  8 / 3428 MEDLINE  
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[PMID]:28587925
[Au] Autor:Mikulic J; Bioley G; Corthésy B
[Ad] Endereço:R&D Laboratory, Division of Immunology and Allergy, CHUV, Centre des Laboratoires d'Epalinges, 1066 Epalinges, Switzerland.
[Ti] Título:SIgA-Shigella Immune Complexes Interact with Dectin-1 and SIGNR3 to Differentially Regulate Mouse Peyer's Patch and Mesenteric Lymph Node Dendritic Cell's Responsiveness.
[So] Source:J Mol Biol;429(15):2387-2400, 2017 Jul 21.
[Is] ISSN:1089-8638
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In addition to contributing to immune exclusion at mucosal surfaces, secretory IgA (SIgA) made of polymeric IgA and secretory component is able to selectively reenter via microfold cells into Peyer's patches (PPs) present along the intestine and to associate with dendritic cells (DCs) of the CD11c CD11b MHCII F4/80 CD8 phenotype in the subepithelial dome region and the draining mesenteric lymph nodes (MLNs). However, the nature of the receptor(s) for SIgA on murine PP and MLN DCs is unknown. We find that glycosylated secretory component moiety and polymeric IgA are both involved in the specific interaction with these cells. Using blocking antibodies and competition experiments, we identify Dectin-1 and specific intercellular adhesion molecule-3 grabbing non-integrin receptor 3 (SIGNR3) as receptors for SIgA. While SIgA-commensal immune complexes (ICs) contribute to local homeostasis upon interaction with mucosal DCs, the picture is less clear for pathogenic agents. We find that in comparison with incubation of Shigella flexneri alone, association of the enteropathogen with SIgA prompts freshly isolated DCs from PPs and MLNs to invert the production of pro- versus non-inflammatory cytokines/chemokines. The sum of the data suggests that in contrast to IgG-based ICs boosting immune reactivity of antigen-presenting cells, SIgA produced during an ongoing immune response can, in addition to its known function of immune exclusion, modulate mucosal DC conditioning via specific interaction with Dectin-1 and SIGNR3.
[Mh] Termos MeSH primário: Complexo Antígeno-Anticorpo/metabolismo
Antígenos CD/metabolismo
Células Dendríticas/imunologia
Imunoglobulina A Secretora/metabolismo
Lectinas Tipo C/metabolismo
Shigella flexneri/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antibacterianos/metabolismo
Antígenos de Bactérias/metabolismo
Citocinas/metabolismo
Linfonodos/imunologia
Camundongos
Nódulos Linfáticos Agregados/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Bacterial); 0 (Antigen-Antibody Complex); 0 (Antigens, Bacterial); 0 (Antigens, CD); 0 (Cytokines); 0 (Immunoglobulin A, Secretory); 0 (Lectins, C-Type); 0 (SIGNR3 protein, mouse); 0 (dectin 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


  9 / 3428 MEDLINE  
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[PMID]:28538737
[Au] Autor:Mendoza A; Fang V; Chen C; Serasinghe M; Verma A; Muller J; Chaluvadi VS; Dustin ML; Hla T; Elemento O; Chipuk JE; Schwab SR
[Ad] Endereço:Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA.
[Ti] Título:Lymphatic endothelial S1P promotes mitochondrial function and survival in naive T cells.
[So] Source:Nature;546(7656):158-161, 2017 06 01.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Effective adaptive immune responses require a large repertoire of naive T cells that migrate throughout the body, rapidly identifying almost any foreign peptide. Because the production of T cells declines with age, naive T cells must be long-lived. However, it remains unclear how naive T cells survive for years while constantly travelling. The chemoattractant sphingosine 1-phosphate (S1P) guides T cell circulation among secondary lymphoid organs, including spleen, lymph nodes and Peyer's patches, where T cells search for antigens. The concentration of S1P is higher in circulatory fluids than in lymphoid organs, and the S1P receptor (S1P R) directs the exit of T cells from the spleen into blood, and from lymph nodes and Peyer's patches into lymph. Here we show that S1P is essential not only for the circulation of naive T cells, but also for their survival. Using transgenic mouse models, we demonstrate that lymphatic endothelial cells support the survival of T cells by secreting S1P via the transporter SPNS2, that this S1P signals through S1P R on T cells, and that the requirement for S1P R is independent of the established role of the receptor in guiding exit from lymph nodes. S1P signalling maintains the mitochondrial content of naive T cells, providing cells with the energy to continue their constant migration. The S1P signalling pathway is being targeted therapeutically to inhibit autoreactive T cell trafficking, and these findings suggest that it may be possible simultaneously to target autoreactive or malignant cell survival.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Tecido Linfoide/citologia
Lisofosfolipídeos/metabolismo
Mitocôndrias/metabolismo
Esfingosina/análogos & derivados
Linfócitos T/citologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte de Ânions/metabolismo
Movimento Celular
Sobrevivência Celular
Feminino
Linfonodos/citologia
Linfonodos/imunologia
Tecido Linfoide/imunologia
Masculino
Camundongos
Camundongos Transgênicos
Nódulos Linfáticos Agregados/citologia
Nódulos Linfáticos Agregados/imunologia
Receptores de Lisoesfingolipídeo/metabolismo
Transdução de Sinais
Esfingosina/metabolismo
Baço/citologia
Baço/imunologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 0 (Spns2 protein, mouse); 26993-30-6 (sphingosine 1-phosphate); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1038/nature22352


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[PMID]:28512157
[Au] Autor:Jinnohara T; Kanaya T; Hase K; Sakakibara S; Kato T; Tachibana N; Sasaki T; Hashimoto Y; Sato T; Watarai H; Kunisawa J; Shibata N; Williams IR; Kiyono H; Ohno H
[Ad] Endereço:Laboratory for Intestinal Ecosystem, Center for Integrative Medical Sciences, Institute of Physical and Chemical Research, Yokohama 230-0045, Japan.
[Ti] Título:IL-22BP dictates characteristics of Peyer's patch follicle-associated epithelium for antigen uptake.
[So] Source:J Exp Med;214(6):1607-1618, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin-22 (IL-22) acts protectively and harmfully on intestinal tissue depending on the situation; therefore, IL-22 signaling needs to be tightly regulated. IL-22 binding protein (IL-22BP) binds IL-22 to inhibit IL-22 signaling. It is expressed in intestinal and lymphoid tissues, although its precise distribution and roles have remained unclear. In this study, we show that IL-22BP is highly expressed by CD11b CD8α dendritic cells in the subepithelial dome region of Peyer's patches (PPs). We found that IL-22BP blocks IL-22 signaling in the follicle-associated epithelium (FAE) covering PPs, indicating that IL-22BP plays a role in regulating the characteristics of the FAE. As expected, FAE of IL-22BP-deficient ( ) mice exhibited altered properties such as the enhanced expression of mucus and antimicrobial proteins as well as prominent fucosylation, which are normally suppressed in FAE. Additionally, mice exhibited the decreased uptake of bacterial antigens into PPs without affecting M cell function. Our present study thus demonstrates that IL-22BP promotes bacterial uptake into PPs by influencing FAE gene expression and function.
[Mh] Termos MeSH primário: Antígenos de Bactérias/imunologia
Epitélio/imunologia
Nódulos Linfáticos Agregados/imunologia
Receptores de Interleucina/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Contagem de Colônia Microbiana
Células Dendríticas/imunologia
Endocitose
Células Epiteliais/imunologia
Interleucinas/metabolismo
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Interleukins); 0 (Receptors, Interleukin); 0 (interleukin-22); 0 (interleukin-22 receptor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160770



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