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[PMID]:28845904
[Au] Autor:Mueller SN
[Ad] Endereço:Department of Microbiology and Immunology, the University of Melbourne, at the Peter Doherty Institute for Infection and Immunity, Melbourne, Australia.
[Ti] Título:Spreading the load: Antigen transfer between migratory and lymph node-resident dendritic cells promotes T-cell priming.
[So] Source:Eur J Immunol;47(10):1798-1801, 2017 Oct.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DC) are specialized in the processing and presentation of antigen for the activation of lymphocytes. Multiple subsets of DCs exist with distinct functions and roles in the initiation of immune responses. DCs found within tissues acquire antigens or become infected by pathogens and migrate to local draining lymph nodes (LN) where they can directly stimulate T cells. These migratory DCs can also transfer antigens to LN-resident DCs and may indirectly enhance T cell priming. In this issue of the European Journal of Immunology, Gurevich et al. [Eur. J. Immunol. 2017. 47: 1802-1818] elegantly demonstrate the influence of the transfer of antigen from migratory DCs to resident DCs on the dynamics of CD8 T-cell priming in mice. Using both in vitro imaging to visualise antigen dissemination and intravital 2-photon microscopy to track T cell clustering with migratory and resident DCs, antigen-donor DC were found to efficiently distribute antigen to recipient DC. This process, which involved LFA-1, enhanced the recruitment of CD8 T cells into the response and rescued priming when DCs were impaired in presentation capacity. Together, these findings shed light on the dynamics of the transfer of antigens between DCs in vivo for the efficient priming of cytotoxic T cell responses.
[Mh] Termos MeSH primário: Apresentação do Antígeno
Linfócitos T CD8-Positivos/imunologia
Células Dendríticas/imunologia
[Mh] Termos MeSH secundário: Movimento Celular
Células Dendríticas/fisiologia
Microscopia Intravital
Linfonodos/citologia
Antígeno-1 Associado à Função Linfocitária/imunologia
Antígeno-1 Associado à Função Linfocitária/metabolismo
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphocyte Function-Associated Antigen-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747248


  2 / 3871 MEDLINE  
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[PMID]:28784685
[Au] Autor:Verma NK; Kelleher D
[Ad] Endereço:Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 636921, Singapore; and nkverma@ntu.edu.sg dermot.kelleher@ubc.ca.
[Ti] Título:Not Just an Adhesion Molecule: LFA-1 Contact Tunes the T Lymphocyte Program.
[So] Source:J Immunol;199(4):1213-1221, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The α ß integrin LFA-1 is known to play a key role in T lymphocyte migration, which is necessary to mount a local immune response, and is also the main driver of autoimmune diseases. This migration-triggering signaling process in T cells is tightly regulated to permit an immune response that is appropriate to the local trigger, as well as to prevent deleterious tissue-damaging bystander effects. Emerging evidence shows that, in addition to prompting a diverse range of downstream signaling cascades, LFA-1 stimulation in T lymphocytes modulates gene-transcription programs, including genetic signatures of TGF-ß and Notch pathways, with multifactorial biological outcomes. This review highlights recent findings and discusses molecular mechanisms by which LFA-1 signaling influence T lymphocyte differentiation into the effector subsets Th1, Th17, and induced regulatory T cells. We argue that LFA-1 contact with a cognate ligand, such as ICAM-1, independent of the immune synapse activates a late divergence in T cells' effector phenotypes, hence fine-tuning their functioning.
[Mh] Termos MeSH primário: Ativação Linfocitária
Antígeno-1 Associado à Função Linfocitária/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Diferenciação Celular
Seres Humanos
Molécula 1 de Adesão Intercelular/imunologia
Molécula 1 de Adesão Intercelular/metabolismo
Antígeno-1 Associado à Função Linfocitária/genética
Antígeno-1 Associado à Função Linfocitária/metabolismo
Camundongos
Fenótipo
Transdução de Sinais
Células Th1/imunologia
Células Th1/fisiologia
Células Th17/imunologia
Células Th17/fisiologia
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Lymphocyte Function-Associated Antigen-1); 0 (Transforming Growth Factor beta); 126547-89-5 (Intercellular Adhesion Molecule-1)
[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:170809
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700495


  3 / 3871 MEDLINE  
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[PMID]:28714582
[Au] Autor:Kragstrup TW; Juul-Madsen K; Christiansen SH; Zhang X; Krog J; Vorup-Jensen T; Kjaergaard AG
[Ad] Endereço:Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark.
[Ti] Título:Altered levels of soluble CD18 may associate immune mechanisms with outcome in sepsis.
[So] Source:Clin Exp Immunol;190(2):258-267, 2017 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The pathogenesis of sepsis involves a dual inflammatory response, with a hyperinflammatory phase followed by, or in combination with, a hypoinflammatory phase. The adhesion molecules lymphocyte function-associated antigen (LFA-1) (CD11a/CD18) and macrophage-1 (Mac-1) (CD11b/CD18) support leucocyte adhesion to intercellular adhesion molecules and phagocytosis through complement opsonization, both processes relevant to the immune response during sepsis. Here, we investigate the role of soluble (s)CD18 in sepsis with emphasis on sCD18 as a mechanistic biomarker of immune reactions and outcome of sepsis. sCD18 levels were measured in 15 septic and 15 critically ill non-septic patients. Fifteen healthy volunteers served as controls. CD18 shedding from human mononuclear cells was increased in vitro by several proinflammatory mediators relevant in sepsis. sCD18 inhibited cell adhesion to the complement fragment iC3b, which is a ligand for CD11b/CD18, also known as Mac-1 or complement receptor 3. Serum sCD18 levels in sepsis non-survivors displayed two distinct peaks permitting a partitioning into two groups, namely sCD18 'high' and sCD18 'low', with median levels of sCD18 at 2158 mU/ml [interquartile range (IQR) 2093-2811 mU/ml] and 488 mU/ml (IQR 360-617 mU/ml), respectively, at the day of intensive care unit admission. Serum sCD18 levels partitioned sepsis non-survivors into one group of 'high' sCD18 and low CRP and another group with 'low' sCD18 and high C-reactive protein. Together with the mechanistic data generated in vitro, we suggest the partitioning in sCD18 to reflect a compensatory anti-inflammatory response syndrome and hyperinflammation, respectively, manifested as part of sepsis.
[Mh] Termos MeSH primário: Antígenos CD18/sangue
Sepse/imunologia
Choque Séptico/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/sangue
Adesão Celular
Feminino
Seres Humanos
Unidades de Terapia Intensiva
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/imunologia
Lipopolissacarídeos/imunologia
Antígeno-1 Associado à Função Linfocitária/metabolismo
Antígeno de Macrófago 1/metabolismo
Masculino
Meia-Idade
Sepse/fisiopatologia
Choque Séptico/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD18 Antigens); 0 (Lipopolysaccharides); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Macrophage-1 Antigen)
[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:170718
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13016


  4 / 3871 MEDLINE  
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[PMID]:28637901
[Au] Autor:Borger JG; Morrison VL; Filby A; Garcia C; Uotila LM; Simbari F; Fagerholm SC; Zamoyska R
[Ad] Endereço:Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh EH9 3FL, United Kingdom.
[Ti] Título:Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells.
[So] Source:J Immunol;199(3):874-884, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TCR stimulation by peptide-MHC complexes on APCs requires precise reorganization of molecules into the area of cellular contact to form an immunological synapse from where T cell signaling is initiated. Caveolin (Cav)1, a widely expressed transmembrane protein, is involved in the regulation of membrane composition, cellular polarity and trafficking, and the organization of signal transduction pathways. The presence of Cav1 protein in T cells was identified only recently, and its function in this context is not well understood. We show that Cav1-knockout CD8 T cells have a reduction in membrane cholesterol and sphingomyelin, and upon TCR triggering they exhibit altered morphology and polarity, with reduced effector function compared with Cav1 wild-type CD8 T cells. In particular, redistribution of the ß integrin LFA-1 to the immunological synapse is compromised in Cav1-knockout T cells, as is the ability of LFA-1 to form high-avidity interactions with ICAM-1. Our results identify a role for Cav1 in membrane organization and ß integrin function in primary CD8 T cells.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Caveolina 1/metabolismo
Sinapses Imunológicas/metabolismo
Ativação Linfocitária
Antígeno-1 Associado à Função Linfocitária/metabolismo
Receptores de Antígenos de Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/química
Linfócitos T CD8-Positivos/metabolismo
Caveolina 1/deficiência
Membrana Celular/química
Membrana Celular/imunologia
Membrana Celular/metabolismo
Polaridade Celular/imunologia
Colesterol/análise
Sinapses Imunológicas/química
Sinapses Imunológicas/imunologia
Molécula 1 de Adesão Intercelular/metabolismo
Camundongos
Receptores de Antígenos de Linfócitos T/química
Transdução de Sinais
Esfingomielinas/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caveolin 1); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Receptors, Antigen, T-Cell); 0 (Sphingomyelins); 126547-89-5 (Intercellular Adhesion Molecule-1); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700431


  5 / 3871 MEDLINE  
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[PMID]:28615221
[Au] Autor:Pick R; Begandt D; Stocker TJ; Salvermoser M; Thome S; Böttcher RT; Montanez E; Harrison U; Forné I; Khandoga AG; Coletti R; Weckbach LT; Brechtefeld D; Haas R; Imhof A; Massberg S; Sperandio M; Walzog B
[Ad] Endereço:Department of Cardiovascular Physiology and Pathophysiology, Walter Brendel Center of Experimental Medicine, Biomedical Center, Ludwig-Maximilians-Universität München, Planegg-Martinsried, Germany.
[Ti] Título:Coronin 1A, a novel player in integrin biology, controls neutrophil trafficking in innate immunity.
[So] Source:Blood;130(7):847-858, 2017 Aug 17.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trafficking of polymorphonuclear neutrophils (PMNs) during inflammation critically depends on the ß integrins lymphocyte function-associated antigen 1 (LFA-1) (CD11a/CD18) and macrophage-1 antigen (CD11b/CD18). Here, we identify coronin 1A (Coro1A) as a novel regulator of ß integrins that interacts with the cytoplasmic tail of CD18 and is crucial for induction of PMN adhesion and postadhesion events, including adhesion strengthening, spreading, and migration under flow conditions. Transition of PMN rolling to firm adhesion critically depends on Coro1A by regulating the accumulation of high-affinity LFA-1 in focal zones of adherent cells. Defective integrin affinity regulation in the genetic absence of impairs leukocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with control animals. In a mouse infection model, PMN infiltration into the gastric mucosa is dramatically reduced in mice, resulting in an attenuated gastric inflammation. Thus, Coro1A represents an important novel player in integrin biology, with key functions in PMN trafficking during innate immunity.
[Mh] Termos MeSH primário: 4-Butirolactona/análogos & derivados
Antígenos CD18/metabolismo
Movimento Celular
Imunidade Inata
Neutrófilos/citologia
Neutrófilos/metabolismo
[Mh] Termos MeSH secundário: 4-Butirolactona/metabolismo
Actinas/metabolismo
Animais
Sinalização do Cálcio
Adesão Celular
Gastrite/imunologia
Gastrite/microbiologia
Gastrite/patologia
Helicobacter pylori/fisiologia
Antígeno-1 Associado à Função Linfocitária/metabolismo
Antígeno de Macrófago 1/metabolismo
Camundongos Endogâmicos C57BL
Receptores Acoplados a Proteínas-G/metabolismo
Reologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CD18 Antigens); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Macrophage-1 Antigen); 0 (Receptors, G-Protein-Coupled); 0 (coronin); OL659KIY4X (4-Butyrolactone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-749622


  6 / 3871 MEDLINE  
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[PMID]:28526681
[Au] Autor:Qaqish A; Huang D; Chen CY; Zhang Z; Wang R; Li S; Yang E; Lu Y; Larsen MH; Jacobs WR; Qian L; Frencher J; Shen L; Chen ZW
[Ad] Endereço:Department of Microbiology and Immunology, Center for Primate Biomedical Research, University of Illinois College of Medicine Chicago, Chicago, IL 60612.
[Ti] Título:Adoptive Transfer of Phosphoantigen-Specific γδ T Cell Subset Attenuates Infection in Nonhuman Primates.
[So] Source:J Immunol;198(12):4753-4763, 2017 Jun 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The dominant Vγ2Vδ2 T cell subset recognizes phosphoantigen and exists only in humans and nonhuman primates. Despite the discovery of γδ T cells >30 y ago, a proof-of-concept study has not been done to prove the principle that the Vγ2Vδ2 T cell subset is protective against and other infections. In this study, we used an adoptive cell-transfer strategy to define the protective role of Vγ2Vδ2 T cells in a primate tuberculosis (TB) model. Vγ2Vδ2 T cells for adoptive transfer displayed central/effector memory and mounted effector functions, including the production of anti- cytokines and inhibition of intracellular mycobacteria. They also expressed CXCR3/CCR5/LFA-1 trafficking/tissue-resident phenotypes and consistently trafficked to the airway, where they remained detectable from 6 h through 7 d after adoptive transfer. Interestingly, the test group of macaques receiving transfer of Vγ2Vδ2 T cells at weeks 1 and 3 after high-dose (500 CFU) infection exhibited significantly lower levels of infection burdens in lung lobes and extrapulmonary organs than did the control groups receiving PBLs or saline. Consistently, adoptive transfer of Vγ2Vδ2 T cells attenuated TB pathology and contained lesions primarily in the infection site of the right caudal lung lobe, with no or reduced TB dissemination to other lobes, spleen, or liver/kidney; in contrast, the controls showed widespread TB dissemination. The proof-of-concept finding supports the view that the dominant Vγ2Vδ2 T cell subset may be included in the rational design of a TB vaccine or host-directed therapy.
[Mh] Termos MeSH primário: Transferência Adotiva
Mycobacterium tuberculosis/imunologia
Fosfoproteínas/uso terapêutico
Receptores de Antígenos de Linfócitos T gama-delta/uso terapêutico
Subpopulações de Linfócitos T/imunologia
Tuberculose/imunologia
Tuberculose/terapia
[Mh] Termos MeSH secundário: Animais
Carga Bacteriana
Citocinas/biossíntese
Citocinas/imunologia
Memória Imunológica
Pulmão/imunologia
Pulmão/microbiologia
Antígeno-1 Associado à Função Linfocitária/genética
Antígeno-1 Associado à Função Linfocitária/imunologia
Macaca fascicularis
Fosfoproteínas/administração & dosagem
Fosfoproteínas/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Receptores CCR5/genética
Receptores CCR5/imunologia
Receptores CXCR3/genética
Receptores CXCR3/imunologia
Tuberculose/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Phosphoproteins); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, CCR5); 0 (Receptors, CXCR3)
[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:170521
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602019


  7 / 3871 MEDLINE  
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[PMID]:28515282
[Au] Autor:Klann JE; Remedios KA; Kim SH; Metz PJ; Lopez J; Mack LA; Zheng Y; Ginsberg MH; Petrich BG; Chang JT
[Ad] Endereço:Department of Medicine, University of California San Diego, La Jolla, CA 92093.
[Ti] Título:Talin Plays a Critical Role in the Maintenance of the Regulatory T Cell Pool.
[So] Source:J Immunol;198(12):4639-4651, 2017 Jun 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Talin, a cytoskeletal protein essential in mediating integrin activation, has been previously shown to be involved in the regulation of T cell proliferation and function. In this study, we describe a role for talin in maintaining the homeostasis and survival of the regulatory T (Treg) cell pool. T cell-specific deletion of talin in mice resulted in spontaneous lymphocyte activation, primarily due to numerical and functional deficiencies of Treg cells in the periphery. Peripheral talin-deficient Treg cells were unable to maintain high expression of IL-2Rα, resulting in impaired IL-2 signaling and ultimately leading to increased apoptosis through downregulation of prosurvival proteins Bcl-2 and Mcl-1. The requirement for talin in maintaining high IL-2Rα expression by Treg cells was due, in part, to integrin LFA-1-mediated interactions between Treg cells and dendritic cells. Collectively, our data suggest a critical role for talin in Treg cell-mediated maintenance of immune homeostasis.
[Mh] Termos MeSH primário: Homeostase
Ativação Linfocitária
Transdução de Sinais
Linfócitos T Reguladores/imunologia
Talina/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Células Dendríticas/imunologia
Genes bcl-2
Interleucina-2/imunologia
Interleucina-2/metabolismo
Subunidade alfa de Receptor de Interleucina-2/genética
Subunidade alfa de Receptor de Interleucina-2/imunologia
Antígeno-1 Associado à Função Linfocitária/imunologia
Antígeno-1 Associado à Função Linfocitária/metabolismo
Camundongos
Proteína de Sequência 1 de Leucemia de Células Mieloides/genética
Linfócitos T Reguladores/fisiologia
Talina/deficiência
Talina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Mcl1 protein, mouse); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Talin)
[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:170519
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601165


  8 / 3871 MEDLINE  
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[PMID]:28511090
[Au] Autor:Käfer R; Schrick K; Schmidtke L; Montermann E; Hobernik D; Bros M; Chen CY; Kleinert H; Pautz A
[Ad] Endereço:Department of Pharmacology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.
[Ti] Título:Inactivation of the KSRP gene modifies collagen antibody induced arthritis.
[So] Source:Mol Immunol;87:207-216, 2017 Jul.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The KH type splicing regulatory protein (KSRP) is a nucleic acid binding protein, which negatively regulates the stability and/or translatability of many mRNA species encoding immune-relevant proteins. As KSRP is expressed in immune cells including T and B cells, neutrophils, macrophages and dendritic cells, we wanted to analyze its importance for the development of autoimmune diseases. We chose collagen antibody-induced arthritis (CAIA) as an appropriate autoimmune disease mouse model in which neutrophils and macrophages constitute the main effector cell populations. We compared arthritis induction in wild type (WT) and KSRP mice and paws were taken for histological sections and qPCR analysis. Furthermore, we determined the frequencies of spleen immune cells by flow cytometry. Cytokine levels in spleen cell supernatants were determined by cytometric bead array analyses (CBA). After CAIA induction we unexpectedly observed in WT animals much stronger swelling of the paws than in KSRP mice. In accordance, histological staining of paw sections of KSRP animals revealed much lower frequencies of infiltrating immune cells in the joints compared to WT animals. Furthermore, CAIA-treatment resulted in reduced expression of several inflammatory factors (like CXCL-1, iNOS, TNF-α and S100A8) as well as immune cell marker genes (e.g. LFA-1, CD68, Ly6G) in the joints of KSRP mice. Spleen cells of KSRP mice showed lower frequencies of myeloid cells. On cytokine level IFN-γ production was increased in spleen cells of KSRP mice compared to WT samples. These data surprisingly suggest that the absence of KSRP protects against the induction of inflammatory arthritis.
[Mh] Termos MeSH primário: Anticorpos/metabolismo
Artrite Experimental/genética
Colágeno/metabolismo
Proteínas de Ligação a RNA/genética
Transativadores/genética
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Antígenos Ly/metabolismo
Artrite Experimental/metabolismo
Calgranulina A/metabolismo
Quimiocina CXCL1/metabolismo
Citocinas/metabolismo
Inflamação/genética
Inflamação/metabolismo
Interferon gama/metabolismo
Antígeno-1 Associado à Função Linfocitária/metabolismo
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Óxido Nítrico Sintase Tipo II/metabolismo
RNA Mensageiro/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Antigens, Ly); 0 (CD68 antigen, human); 0 (Calgranulin A); 0 (Chemokine CXCL1); 0 (Cytokines); 0 (KSRP protein, mouse); 0 (Lymphocyte Function-Associated Antigen-1); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 0 (Trans-Activators); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma); 9007-34-5 (Collagen); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE


  9 / 3871 MEDLINE  
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[PMID]:28400196
[Au] Autor:Gonsky R; Fleshner P; Deem RL; Biener-Ramanujan E; Li D; Potdar AA; Bilsborough J; Yang S; McGovern DPB; Targan SR
[Ad] Endereço:F. Widjaja Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, California.
[Ti] Título:Association of Ribonuclease T2 Gene Polymorphisms With Decreased Expression and Clinical Characteristics of Severity in Crohn's Disease.
[So] Source:Gastroenterology;153(1):219-232, 2017 Jul.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Variants in the tumor necrosis factor superfamily member 15 gene (TNFSF15, also called TL1A) have been associated with risk for inflammatory bowel disease (IBD). TL1A affects expression of multiple cytokines to promote mucosal inflammation. Little is known about the TL1A-response pathways that regulate cytokine expression. We investigated T-cell gene expression patterns to determine the mechanisms by which TL1A regulates cytokine production, and whether these associate with outcomes of patients with Crohn's disease (CD). METHODS: Peripheral T cells isolated from normal donors were cultured with TL1A. We performed gene expression profile analysis by RNA sequencing of subsets of interferon gamma (IFNG)-producing and non-producing cells purified by flow cytometry. Unsupervised hierarchical clustering analysis was used to identify gene expression differences between these subsets. Ribonuclease T2 gene (RNASET2) expression and methylation were assessed by quantitative trait loci analyses. Clinical characteristics of patients (complications, resistance to therapy, and recurrence time) were associated with single nucleotide polymorphisms in RNASET2. We performed motif screening to identify polymorphisms that disrupt transcription factor binding sites. Levels of RNASET2 were knocked down with small interfering RNA in CD4 T cells and the effect on protein expression was determined by proteomic analysis and cytokine production. Cell aggregation was measured by flow cytometry. RESULTS: We identified 764 genes with at least a 2-fold difference in TL1A-mediated expression between IFNG-secreting and non-secreting T cells (P < 1 × 10 ). Many of these genes were located near IBD susceptibility variants. RNASET2 was the only IBD risk-associated gene with >5-fold down-regulation in the IFNG-secreting subset. RNASET2 disease risk variants were associated with decreased expression in peripheral and mucosal tissues and DNA hypermethylation in CD patients requiring surgical intervention. RNASET2 disease risk variants were associated in CD patients with more complicated disease or resistance to therapy, defined in part by failed response to treatment, increased length of intestinal resection, shorter time to repeat surgery, and high Rutgeerts score (>2) in postoperative endoscopy. The RNASET2 variant rs2149092 was predicted to disrupt a consensus binding site for the transcription factor ETS within an enhancer region. Expression of RNASET2 correlated with expression of ETS. RNASET2 knockdown in T cells increased expression of IFNG and intercellular adhesion molecule 1 (ICAM1) and induced T-cell aggregation. A blocking antibody against (ILFA1), disrupting the lymphocyte function-associated antigen 1-intercellular adhesion molecule 1 interaction, reduced T-cell production of IFNG. CONCLUSIONS: We identified decreased expression of RNASET2 as a component of TL1A-mediated increase in production of IFNG and as a potential biomarker for patients with severe CD. Further study of the role of RNASET2 in regulating mucosal inflammation may lead to development of novel therapeutic targets.
[Mh] Termos MeSH primário: Doença de Crohn/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Interferon gama/secreção
Ribonucleases/genética
Linfócitos T/efeitos dos fármacos
Membro 15 da Superfamília de Ligantes de Fatores de Necrose Tumoral/farmacologia
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Alelos
Agregação Celular
Células Cultivadas
Doença de Crohn/cirurgia
Metilação de DNA
Regulação para Baixo
Inativação Gênica
Seres Humanos
Molécula 1 de Adesão Intercelular/genética
Mucosa Intestinal/metabolismo
Antígeno-1 Associado à Função Linfocitária/imunologia
Polimorfismo de Nucleotídeo Único
Proteínas Proto-Oncogênicas c-ets/genética
Índice de Gravidade de Doença
Linfócitos T/secreção
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ICAM1 protein, human); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Proto-Oncogene Proteins c-ets); 0 (TNFSF15 protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 15); 0 (Tumor Suppressor Proteins); 126547-89-5 (Intercellular Adhesion Molecule-1); 82115-62-6 (Interferon-gamma); EC 3.1.- (Ribonucleases); EC 3.1.27.- (RNASET2 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE


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[PMID]:28348273
[Au] Autor:Lagarrigue F; Gertler FB; Ginsberg MH; Cantor JM
[Ad] Endereço:Department of Medicine, University of California San Diego, La Jolla, CA 92093; and.
[Ti] Título:Cutting Edge: Loss of T Cell RIAM Precludes Conjugate Formation with APC and Prevents Immune-Mediated Diabetes.
[So] Source:J Immunol;198(9):3410-3415, 2017 May 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rap1-interacting adaptor molecule (RIAM) is a Rap1 effector that mediates the recruitment of talin to integrins, thereby supporting their activation. In this study, we investigated the role of RIAM in an adoptive transfer model for type I diabetes and report that RIAM expression in T cells is necessary for diabetes development. Loss of RIAM did not prevent lymphocyte recruitment to draining lymph nodes 24 h after transfer, but it was required for Ag-driven proliferation and cytotoxic killing. RIAM is recruited to immune synapses along with talin and LFA-1, and loss of RIAM profoundly suppresses Ag-dependent conjugate formation in primary naive and effector T cells. These data identify the requirement of RIAM for formation of immunological synapses and in resulting T cell functions in autoimmunity. Moreover, because RIAM-null mice are healthy, fertile, and display no bleeding abnormalities, our results identify RIAM and its regulators as potential targets for therapies of T cell-mediated autoimmunity.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Células Apresentadoras de Antígenos/imunologia
Diabetes Mellitus Tipo 1/imunologia
Antígeno-1 Associado à Função Linfocitária/metabolismo
Proteínas de Membrana/metabolismo
Linfócitos T/imunologia
Talina/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Transferência Adotiva
Animais
Proliferação Celular/genética
Células Cultivadas
Citotoxicidade Imunológica/genética
Seres Humanos
Sinapses Imunológicas/imunologia
Proteínas de Membrana/genética
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Linfócitos T/transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Membrane Proteins); 0 (RIAM protein, mouse); 0 (Talin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601743



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