Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.408.100 [Categoria DeCS]
Referências encontradas : 1189 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 119 ir para página                         

  1 / 1189 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29203246
[Au] Autor:Popielarski M; Ponamarczuk H; Stasiak M; Michalec L; Bednarek R; Studzian M; Pulaski L; Swiatkowska M
[Ad] Endereço:Department of Cytobiology and Proteomics, Medical University of Lodz, 6/8 Mazowiecka St., 92-215 Lodz, Poland. Electronic address: marcin.popielarski@umed.lodz.pl.
[Ti] Título:The role of Protein Disulfide Isomerase and thiol bonds modifications in activation of integrin subunit alpha11.
[So] Source:Biochem Biophys Res Commun;495(2):1635-1641, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Integrins belong to a family of transmembrane receptors that mediate cell migration and adhesion to ECM. Extracellular domains of integrin heterodimers contain cysteine-rich regions, which are potential sites of thiol-disulfide exchanges. Rearrangements of extracellular disulfide bonds regulate activation of integrin receptors by promoting transition from an inactive state into a ligand-binding competent state. Modifications of integrin disulfide bonds dependent on oxidation-reduction can be mediated by Protein Disulfide Isomerse (PDI). This paper provides evidences that binding to integrin ligands initiate changes in free thiol pattern on cell surface and that thiol-disulfide exchange mediated by PDI leads to activation of integrin subunit α11. By employing co-immunoprecipitation and confocal microscopy analysis we showed that α11ß1 and PDI create complexes bounded by disulfide bonds. Using surface plasmon resonance we provide biochemical evidence that PDI can interact directly with integrin subunit α11.
[Mh] Termos MeSH primário: Cadeias alfa de Integrinas/química
Cadeias alfa de Integrinas/metabolismo
Isomerases de Dissulfetos de Proteínas/metabolismo
[Mh] Termos MeSH secundário: Adesão Celular
Movimento Celular
Células Cultivadas
Seres Humanos
Imunoprecipitação
Integrina beta1/química
Integrina beta1/metabolismo
Microscopia Confocal
Domínios e Motivos de Interação entre Proteínas
Compostos de Sulfidrila/química
Compostos de Sulfidrila/metabolismo
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ITGA11 protein, human); 0 (Integrin alpha Chains); 0 (Integrin beta1); 0 (Sulfhydryl Compounds); EC 5.3.4.1 (Protein Disulfide-Isomerases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


  2 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27776108
[Au] Autor:Hombrink P; Helbig C; Backer RA; Piet B; Oja AE; Stark R; Brasser G; Jongejan A; Jonkers RE; Nota B; Basak O; Clevers HC; Moerland PD; Amsen D; van Lier RA
[Ad] Endereço:Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Amsterdam, the Netherlands.
[Ti] Título:Programs for the persistence, vigilance and control of human CD8 lung-resident memory T cells.
[So] Source:Nat Immunol;17(12):1467-1478, 2016 Dec.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tissue-resident memory T cells (T cells) in the airways mediate protection against respiratory infection. We characterized T cells expressing integrin α (CD103) that reside within the epithelial barrier of human lungs. These cells had specialized profiles of chemokine receptors and adhesion molecules, consistent with their unique localization. Lung T cells were poised for rapid responsiveness by constitutive expression of deployment-ready mRNA encoding effector molecules, but they also expressed many inhibitory regulators, suggestive of programmed restraint. A distinct set of transcription factors was active in CD103 T cells, including Notch. Genetic and pharmacological experiments with mice revealed that Notch activity was required for the maintenance of CD103 T cells. We have thus identified specialized programs underlying the residence, persistence, vigilance and tight control of human lung T cells.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/fisiologia
Memória Imunológica
Vírus da Influenza A Subtipo H3N2/imunologia
Pulmão/imunologia
Infecções por Orthomyxoviridae/imunologia
Receptor Notch1/metabolismo
Receptor Notch2/metabolismo
Infecções Respiratórias/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Células Cultivadas
Feminino
Seres Humanos
Cadeias alfa de Integrinas/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Meia-Idade
Receptor Notch1/genética
Receptor Notch2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Integrin alpha Chains); 0 (Notch1 protein, mouse); 0 (Notch2 protein, mouse); 0 (Receptor, Notch1); 0 (Receptor, Notch2); 0 (alpha E integrins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3589


  3 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28869696
[Au] Autor:Nathan AA; Dixit M; Babu S; Balakrishnan AS
[Ad] Endereço:Department of Genetic Engineering, School of Biotechnology, Madurai Kamaraj University, Madurai, India.
[Ti] Título:Comparison and functional characterisation of peripheral blood mononuclear cells isolated from filarial lymphoedema and endemic normals of a South Indian population.
[So] Source:Trop Med Int Health;22(11):1414-1427, 2017 Nov.
[Is] ISSN:1365-3156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The underlying problem in lymphatic filariasis is irreversible swelling of the limbs (lymphoedema), which is a unique feature of lymphatic insufficiency. It is still unclear whether the natural ability of lymphatics to form functional lymphatic vasculature is achieved or attenuated in the lymphoedemal pathology. Clinical studies have clearly shown that circulating lymphatic progenitors (CLPs), a subset of bone marrow-derived mononuclear cells (PBMCs), contribute to post-natal lymph vasculogenesis. CLP-based revascularisation could be a promising strategy to bypass the endothelial disruption and damage incurred by the filarial parasites. Thus our aim was to compare and characterise the functional prowess of PBMCs in physiological and lymphoedemal pathology. METHODS: PBMCs were isolated from venous blood sample from drug-naive endemic normals (EN) and drug-deprived filarial lymphoedema (FL) individuals using density gradient centrifugation. Adhesion, transwell migration and in vitro matrigel assays were employed to characterise the lymphvasculogenic potential of PBMCs. CLPs were phenotypically characterised using flow cytometry; expression levels of lymphatic markers and inflammatory cytokines were quantified using qRT-PCR and ELISA, respectively. RESULTS: PBMCs from FL group display poor adherence to fibronectin (P = 0.040), reduced migration towards SDF-1α (P = 0.035), impaired tubular network (P = 0.004) and branching point (P = 0.048) formation. The PBMC mRNA expression of VEGFR3 (P = 0.039) and podoplanin (P = 0.050) was elevated, whereas integrin α9 (P = 0.046) was inhibited in FL individuals; additionally, the surface expression of CD34 (P = 0.048) was significantly reduced in the FL group compared to the EN group. CONCLUSION: PBMCs from filarial lymphoedema show defective and dysregulated lymphvasculogenic function compared to endemic normals.
[Mh] Termos MeSH primário: Filariose Linfática/patologia
Leucócitos Mononucleares/fisiologia
Linfedema
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD34/sangue
Movimento Celular
Quimiocina CXCL12/sangue
Filariose Linfática/sangue
Doenças Endêmicas
Feminino
Fibronectinas/sangue
Seres Humanos
Índia
Cadeias alfa de Integrinas/sangue
Linfedema/sangue
Linfedema/etiologia
Masculino
Glicoproteínas de Membrana
Meia-Idade
RNA Mensageiro/metabolismo
Valores de Referência
Receptor 3 de Fatores de Crescimento do Endotélio Vascular/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Chemokine CXCL12); 0 (Fibronectins); 0 (Integrin alpha Chains); 0 (Membrane Glycoproteins); 0 (PDPN protein, human); 0 (RNA, Messenger); 0 (integrin alpha9); EC 2.7.10.1 (FLT4 protein, human); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE
[do] DOI:10.1111/tmi.12969


  4 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28854563
[Au] Autor:Lemma SA; Kuusisto M; Haapasaari KM; Sormunen R; Lehtinen T; Klaavuniemi T; Eray M; Jantunen E; Soini Y; Vasala K; Böhm J; Salokorpi N; Koivunen P; Karihtala P; Vuoristo J; Turpeenniemi-Hujanen T; Kuittinen O
[Ad] Endereço:Department of Oncology and Radiotherapy, Medical Research Center Oulu, Oulu University Hospital, University of Oulu, Kajaanintie 50, 90220 Oulu, Finland.
[Ti] Título:Integrin alpha 10, CD44, PTEN, cadherin-11 and lactoferrin expressions are potential biomarkers for selecting patients in need of central nervous system prophylaxis in diffuse large B-cell lymphoma.
[So] Source:Carcinogenesis;38(8):812-820, 2017 Aug 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Central nervous system (CNS) relapse is a devastating complication that occurs in about 5% of diffuse large B-cell lymphoma (DLBCL) patients. Currently, there are no predictive biological markers. We wanted to study potential biomarkers of CNS tropism that play a role in adhesion, migration and/or in the regulation of inflammatory responses. The expression levels of ITGA10, CD44, PTEN, cadherin-11, CDH12, N-cadherin, P-cadherin, lactoferrin and E-cadherin were studied with IHC and IEM. GEP was performed to see whether found expressional changes are regulated at DNA/RNA level. IHC included 96 samples of primary CNS lymphoma (PCNSL), secondary CNS lymphoma (sCNSL) and systemic DLBCL (sDLBCL). IEM included two PCNSL, one sCNSL, one sDLBCL and one reactive lymph node samples. GEP was performed on two DLBCL samples, one with and one without CNS relapse. CNS disease was associated with enhanced expression of cytoplasmic and membranous ITGA10 and nuclear PTEN (P < 0.0005, P = 0.002, P = 0.024, respectively). sCNSL presented decreased membranous CD44 and nuclear and cytoplasmic cadherin-11 expressions (P = 0.001, P = 0.006, P = 0.048, respectively). In PCNSL lactoferrin expression was upregulated (P < 0.0005). IEM results were mainly supportive of the IHC results. In GEP CD44, cadherin-11, lactoferrin and E-cadherin were under-expressed in CNS disease. Our results are in line with previous studies, where gene expressions in extracellular matrix and adhesion-related pathways are altered in CNS lymphoma. This study gives new information on the DLBCL CNS tropism. If further verified, these markers might become useful in predicting CNS relapses.
[Mh] Termos MeSH primário: Caderinas/genética
Doenças do Sistema Nervoso Central/genética
Receptores de Hialuronatos/genética
Cadeias alfa de Integrinas/genética
Lactoferrina/genética
Linfoma Difuso de Grandes Células B/genética
PTEN Fosfo-Hidrolase/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/genética
Caderinas/biossíntese
Sistema Nervoso Central/patologia
Doenças do Sistema Nervoso Central/etiologia
Doenças do Sistema Nervoso Central/patologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Receptores de Hialuronatos/biossíntese
Cadeias alfa de Integrinas/biossíntese
Lactoferrina/biossíntese
Linfonodos/metabolismo
Linfonodos/patologia
Linfoma Difuso de Grandes Células B/complicações
Linfoma Difuso de Grandes Células B/patologia
Masculino
Meia-Idade
PTEN Fosfo-Hidrolase/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD44 protein, human); 0 (Cadherins); 0 (Hyaluronan Receptors); 0 (Integrin alpha Chains); 0 (integrin alpha 10); 156621-71-5 (osteoblast cadherin); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human); EC 3.4.21.- (Lactoferrin)
[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:170901
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx061


  5 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28760813
[Au] Autor:Skeath JB; Wilson BA; Romero SE; Snee MJ; Zhu Y; Lacin H
[Ad] Endereço:Department of Genetics, Washington University School of Medicine, 4523 Clayton Avenue, St Louis, MO 63110, USA jskeath@genetics.wustl.edu.
[Ti] Título:The extracellular metalloprotease AdamTS-A anchors neural lineages in place within and preserves the architecture of the central nervous system.
[So] Source:Development;144(17):3102-3113, 2017 09 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The extracellular matrix (ECM) regulates cell migration and sculpts organ shape. AdamTS proteins are extracellular metalloproteases known to modify ECM proteins and promote cell migration, but demonstrated roles for AdamTS proteins in regulating CNS structure and ensuring cell lineages remain fixed in place have not been uncovered. Using forward genetic approaches in , we find that reduction of function induces both the mass exodus of neural lineages out of the CNS and drastic perturbations to CNS structure. Expressed and active in surface glia, acts in parallel to and in opposition to / and - to keep CNS lineages rooted in place and to preserve the structural integrity of the CNS. / and - are known to promote tissue stiffness and oppose the function of , which reduces tissue stiffness. Our work supports a model in which AdamTS-A anchors cells in place and preserves CNS architecture by reducing tissue stiffness.
[Mh] Termos MeSH primário: Linhagem da Célula
Sistema Nervoso Central/citologia
Proteínas de Drosophila/metabolismo
Matriz Extracelular/metabolismo
Neurônios/citologia
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Alelos
Animais
Membrana Basal/metabolismo
Colágeno Tipo IV/metabolismo
Drosophila melanogaster/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Cadeias alfa de Integrinas/metabolismo
Mutação/genética
Neuroglia/citologia
Neuroglia/metabolismo
Fenótipo
Frações Subcelulares/metabolismo
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type IV); 0 (Drosophila Proteins); 0 (Integrin alpha Chains); 0 (if protein, Drosophila); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1242/dev.145854


  6 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28628641
[Au] Autor:Bernatchez E; Langlois A; Brassard J; Flamand N; Marsolais D; Blanchet MR
[Ad] Endereço:Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, Quebec, Quebec, Canada.
[Ti] Título:Hypersensitivity pneumonitis onset and severity is regulated by CD103 dendritic cell expression.
[So] Source:PLoS One;12(6):e0179678, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Pulmonary dendritic cells drive lung responses to foreign antigens, including Saccharopolyspora rectivirgula, a causative agent of hypersensitivity pneumonitis. While the airway inflammatory mechanisms involved in hypersensitivity pneumonitis are well described, the mechanisms leading to the break in homeostasis and hypersensitivity pneumonitis onset are not well-described, and could involve CD103+ dendritic cells, which are found at baseline and during inflammatory responses in the lung. However, recent demonstration of the ability of CD103+ dendritic cells to induce inflammatory responses starkly contrasts with their classically described role as regulatory cells. These discrepancies may be attributable to the lack of current information on the importance of CD103 expression and modulation on these cells during inflammatory episodes. METHODS: To verify the importance of CD103 expression in the regulation of hypersensitivity pneumonitis, wild-type and Cd103-/- mice were exposed intranasally to S. rectivirgula and airway inflammation was quantified. Surface expression of CD103 in response to S. rectivirgula exposure was studied and cell transfers were used to determine the relative importance of CD103 expression on dendritic cells and T cells in regulating the inflammation in hypersensitivity pneumonitis. RESULTS: Cd103-/- mice developed an exacerbated inflammatory response as early as 18h following S. rectivirgula exposure. CD103 expression on dendritic cells was downregulated quickly following S. rectivirgula exposure, and cell transfers demonstrated that CD103 expression on dendritic cells specifically (and not T cells) regulates the onset and severity of this response. CONCLUSION: All in all, we demonstrate that CD103 expression by dendritic cells, but not T cells, is crucial for homeostasis maintenance and the regulation of the TH17 airway inflammatory response in hypersensitivity pneumonitis.
[Mh] Termos MeSH primário: Alveolite Alérgica Extrínseca/patologia
Antígenos CD/metabolismo
Células Dendríticas/metabolismo
Cadeias alfa de Integrinas/metabolismo
[Mh] Termos MeSH secundário: Alveolite Alérgica Extrínseca/imunologia
Alveolite Alérgica Extrínseca/microbiologia
Animais
Antígenos de Bactérias/imunologia
Antígenos CD/genética
Líquido da Lavagem Broncoalveolar/citologia
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD8-Positivos/citologia
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/metabolismo
Citocinas/metabolismo
Células Dendríticas/citologia
Células Dendríticas/imunologia
Modelos Animais de Doenças
Regulação para Baixo
Imunoglobulina G/sangue
Imunoglobulina G/imunologia
Cadeias alfa de Integrinas/deficiência
Cadeias alfa de Integrinas/genética
Leucócitos/citologia
Pulmão/citologia
Pulmão/imunologia
Pulmão/patologia
Camundongos
Camundongos Knockout
Saccharopolyspora/metabolismo
Saccharopolyspora/patogenicidade
Índice de Gravidade de Doença
Baço/citologia
Baço/imunologia
Células Th17/citologia
Células Th17/imunologia
Células Th17/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Antigens, CD); 0 (Cytokines); 0 (Immunoglobulin G); 0 (Integrin alpha Chains); 0 (alpha E integrins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179678


  7 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28628092
[Au] Autor:Ganesan AP; Clarke J; Wood O; Garrido-Martin EM; Chee SJ; Mellows T; Samaniego-Castruita D; Singh D; Seumois G; Alzetani A; Woo E; Friedmann PS; King EV; Thomas GJ; Sanchez-Elsner T; Vijayanand P; Ottensmeier CH
[Ad] Endereço:La Jolla Institute for Allergy &Immunology, La Jolla, California, USA.
[Ti] Título:Tissue-resident memory features are linked to the magnitude of cytotoxic T cell responses in human lung cancer.
[So] Source:Nat Immunol;18(8):940-950, 2017 Aug.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Therapies that boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) have shown promise; however, clinical responses to the immunotherapeutic agents currently available vary considerably, and the molecular basis of this is unclear. We performed transcriptomic profiling of tumor-infiltrating CTLs from treatment-naive patients with lung cancer to define the molecular features associated with the robustness of anti-tumor immune responses. We observed considerable heterogeneity in the expression of molecules associated with activation of the T cell antigen receptor (TCR) and of immunological-checkpoint molecules such as 4-1BB, PD-1 and TIM-3. Tumors with a high density of CTLs showed enrichment for transcripts linked to tissue-resident memory cells (T cells), such as CD103, and CTLs from CD103 tumors displayed features of enhanced cytotoxicity. A greater density of T cells in tumors was predictive of a better survival outcome in lung cancer, and this effect was independent of that conferred by CTL density. Here we define the 'molecular fingerprint' of tumor-infiltrating CTLs and identify potentially new targets for immunotherapy.
[Mh] Termos MeSH primário: Adenocarcinoma/imunologia
Carcinoma de Células Escamosas/imunologia
Neoplasias de Cabeça e Pescoço/imunologia
Memória Imunológica/imunologia
Neoplasias Pulmonares/imunologia
Linfócitos do Interstício Tumoral/imunologia
Linfócitos T Citotóxicos/imunologia
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adulto
Idoso
Idoso de 80 Anos ou mais
Antígenos CD/genética
Carcinoma de Células Escamosas/mortalidade
Feminino
Perfilação da Expressão Gênica
Receptor Celular 2 do Vírus da Hepatite A/genética
Seres Humanos
Imunoterapia
Cadeias alfa de Integrinas/genética
Neoplasias Pulmonares/mortalidade
Linfócitos do Interstício Tumoral/metabolismo
Masculino
Meia-Idade
Prognóstico
Receptor de Morte Celular Programada 1/genética
Receptores de Antígenos de Linfócitos T/genética
Taxa de Sobrevida
Linfócitos T Citotóxicos/metabolismo
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (HAVCR2 protein, human); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (Integrin alpha Chains); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Antigen, T-Cell); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9); 0 (alpha E integrins)
[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:10.1038/ni.3775


  8 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28550205
[Au] Autor:Matsumoto N; Kon S; Nakatsuru T; Miyashita T; Inui K; Saitoh K; Kitai Y; Muromoto R; Kashiwakura JI; Uede T; Matsuda T
[Ad] Endereço:Department of Immunology, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0815, Japan.
[Ti] Título:A Novel α9 Integrin Ligand, XCL1/Lymphotactin, Is Involved in the Development of Murine Models of Autoimmune Diseases.
[So] Source:J Immunol;199(1):82-90, 2017 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The integrin α9ß1 is a key receptor involved in the development of autoimmune diseases. However, the detailed mechanism for the association of α9ß1 integrin with its ligands remains unclear. In this study, we introduce XCL1/lymphotactin, a member of the chemokine family, as a novel ligand for α9 integrin. Using α9 integrin-overexpressing NIH3T3 cells and endogenously α9 integrin-expressing human rhabdomyosarcoma cells, the interaction between XCL1 and α9 integrin was confirmed by pull-down assays. XCL1 enhanced α9 integrin-dependent cell migration of these cells, thus acting on α9 integrin as a chemoattractant. We also analyzed the in vivo function of XCL1 in the development of anti-type II collagen Ab-induced inflammatory arthritis (CAIA) in BALB/c mice and experimental autoimmune encephalomyelitis in C57BL/6 mice, because α9 integrin is involved in these autoimmune disease models. In CAIA, recombinant XCL1 aggravated the disease and this exacerbation was inhibited by an anti-α9 integrin Ab. An XCL1-neutralizing Ab produced in this study also ameliorated CAIA. Furthermore, the XCL1-neutralizing Ab abrogated the disease progression in experimental autoimmune encephalomyelitis. Therefore, to our knowledge this study provides the first in vitro and in vivo evidence that the interaction between XCL1 and α9 integrin has an important role for autoimmune diseases.
[Mh] Termos MeSH primário: Quimiocinas C/imunologia
Quimiocinas C/metabolismo
Encefalomielite Autoimune Experimental/imunologia
Cadeias alfa de Integrinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/imunologia
Artrite Experimental/imunologia
Adesão Celular
Movimento Celular
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/fisiopatologia
Encefalomielite Autoimune Experimental/terapia
Cadeias alfa de Integrinas/imunologia
Ligantes
Camundongos
Camundongos Endogâmicos C57BL
Células NIH 3T3
Rabdomiossarcoma/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Chemokines, C); 0 (Integrin alpha Chains); 0 (Ligands); 0 (XCL1 protein, human); 0 (Xcl1 protein, mouse); 0 (integrin alpha9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601329


  9 / 1189 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28542882
[Au] Autor:Qiang Y; Xu J; Yan C; Jin H; Xiao T; Yan N; Zhou L; An H; Zhou X; Shao Q; Xia S
[Ad] Endereço:Department of Immunology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
[Ti] Título:Butyrate and retinoic acid imprint mucosal-like dendritic cell development synergistically from bone marrow cells.
[So] Source:Clin Exp Immunol;189(3):290-297, 2017 Sep.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Accumulating data show that the phenotypes and functions of distinctive mucosal dendritic cells (DCs) in the gut are regulated by retinoic acid (RA). Unfortunately, the exact role of butyrate in RA-mediated mucosal DC differentiation has not been elucidated thoroughly to date. Mucosal-like dendritic cell differentiation was completed in vitro by culturing bone marrow cells with growth factors [granulocyte-macrophage colony-stimulating factor (GM-CSF/interleukin (IL)-4], RA and/or butyrate. The phenotypes, cytokine secretion, immune functions and levels of retinal dehydrogenase of different DCs were detected using quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) and flow cytometry, respectively. The results showed that RA-induced DCs (RA-DCs) showed mucosal DC properties, including expression of CD103 and gut homing receptor α ß , low proinflammatory cytokine secretion and low priming capability to antigen-specific CD4 T cells. Butyrate-treated RA-DCs (Bu-RA-DCs) decreased CD11c, but increased CD103 and α ß expression. Moreover, the CD4 T priming capability and the levels of retinal dehydrogenase of RA-DCs were suppressed significantly by butyrate. Thus, butyrate and retinoic acid have different but synergistic regulatory functions on mucosal DC differentiation, indicating that immune homeostasis in the gut depends largely upon RA and butyrate to imprint different mucosal DC subsets, both individually and collectively.
[Mh] Termos MeSH primário: Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Butiratos/farmacologia
Linfócitos T CD4-Positivos/imunologia
Células Dendríticas/imunologia
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Antígenos CD/imunologia
Células da Medula Óssea/fisiologia
Antígeno CD11c/genética
Antígeno CD11c/imunologia
Diferenciação Celular
Células Cultivadas
Citocinas/genética
Citocinas/imunologia
Citocinas/secreção
Células Dendríticas/metabolismo
Ensaio de Imunoadsorção Enzimática
Citometria de Fluxo
Fator Estimulador de Colônias de Granulócitos e Macrófagos/farmacologia
Cadeias alfa de Integrinas/genética
Cadeias alfa de Integrinas/imunologia
Integrinas/genética
Integrinas/imunologia
Interleucina-4/farmacologia
Camundongos
Fenótipo
Reação em Cadeia da Polimerase em Tempo Real
Retinal Desidrogenase/genética
Retinal Desidrogenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Butyrates); 0 (CD11c Antigen); 0 (Cytokines); 0 (Integrin alpha Chains); 0 (Integrins); 0 (alpha E integrins); 207137-56-2 (Interleukin-4); 5688UTC01R (Tretinoin); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 1.2.1.36 (Retinal Dehydrogenase)
[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:170526
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12990


  10 / 1189 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28530714
[Au] Autor:Ruscher R; Kummer RL; Lee YJ; Jameson SC; Hogquist KA
[Ad] Endereço:The Department of Laboratory Medicine and Pathology and Center for Immunology, University of Minnesota, Minneapolis, Minnesota, USA.
[Ti] Título:CD8αα intraepithelial lymphocytes arise from two main thymic precursors.
[So] Source:Nat Immunol;18(7):771-779, 2017 Jul.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TCRαß CD4 CD8α CD8ß intestinal intraepithelial lymphocytes (CD8αα IELs) are an abundant population of thymus-derived T cells that protect the gut barrier surface. We sought to better define the thymic IEL precursor (IELp) through analysis of its maturation, localization and emigration. We defined two precursor populations among TCRß CD4 CD8 thymocytes by dependence on the kinase TAK1 and rigorous lineage-exclusion criteria. Those IELp populations included a nascent PD-1 population and a T-bet population that accumulated with age. Both gave rise to intestinal CD8αα IELs after adoptive transfer. The PD-1 IELp population included more strongly self-reactive clones and was largely restricted by classical major histocompatibility complex (MHC) molecules. Those cells localized to the cortex and efficiently emigrated in a manner dependent on the receptor S1PR1. The T-bet IELp population localized to the medulla, included cells restricted by non-classical MHC molecules and expressed the receptor NK1.1, the integrin CD103 and the chemokine receptor CXCR3. The two IELp populations further differed in their use of the T cell antigen receptor (TCR) α-chain variable region (V ) and ß-chain variable region (V ). These data provide a foundation for understanding the biology of CD8αα IELs.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Mucosa Intestinal/imunologia
Células Precursoras de Linfócitos T/imunologia
Timócitos/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Transferência Adotiva
Animais
Antígenos CD
Antígenos Ly/imunologia
Antígenos CD8/imunologia
Linhagem da Célula
Movimento Celular/imunologia
Citometria de Fluxo
Imunofluorescência
Antígenos de Histocompatibilidade/imunologia
Imunidade nas Mucosas/imunologia
Cadeias alfa de Integrinas
Mucosa Intestinal/citologia
Linfócitos
Camundongos
Subfamília B de Receptores Semelhantes a Lectina de Células NK/imunologia
Fenótipo
Receptor de Morte Celular Programada 1/imunologia
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Receptores CXCR3
Receptores de Lisoesfingolipídeo/imunologia
Proteínas com Domínio T-Box/imunologia
Timócitos/citologia
Timo/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Ly); 0 (CD8 Antigens); 0 (CD8 antigen, alpha chain); 0 (Cxcr3 protein, mouse); 0 (Histocompatibility Antigens); 0 (Integrin alpha Chains); 0 (Klrb1c protein, mouse); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Receptors, CXCR3); 0 (Receptors, Lysosphingolipid); 0 (S1PR1 protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 0 (alpha E integrins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3751



página 1 de 119 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde