Base de dados : MEDLINE
Pesquisa : D12.776.395.550.200.074.875 [Categoria DeCS]
Referências encontradas : 1343 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 135 ir para página                         

  1 / 1343 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29324844
[Au] Autor:Barakat DJ; Suresh R; Barberi T; Pienta KJ; Simons BW; Friedman AD
[Ad] Endereço:Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
[Ti] Título:Absence of myeloid Klf4 reduces prostate cancer growth with pro-atherosclerotic activation of tumor myeloid cells and infiltration of CD8 T cells.
[So] Source:PLoS One;13(1):e0191188, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The microenvironment of prostate cancer often includes abundant tumor-associated macrophages (TAMs), with their acquisition of an M2 phenotype correlating with local aggressiveness and metastasis. Tumor-derived M-CSF contributes to TAM M2 polarization, and M-CSF receptor inhibition slows prostate cancer growth in model systems. As additional cytokines can direct TAM M2 polarization, targeting downstream transcription factors could avoid resistance. Klf4 and C/EBPß each contribute to monocyte development, and reduced expression of macrophage Klf4 or C/EBPß favors their adoption of a pro-inflammatory M1 state. We find that a Hi-Myc C57BL/6 prostate cancer line grows more slowly in syngeneic Klf4(f/f);Lys-Cre compared with Klf4(f/f) mice when inoculated subcutaneously, but grows equally rapidly in C/EBPß(f/f);Lys-Cre and C/EBPß(f/f) hosts. In the absence of myeloid Klf4, TAMs have reduced expression of surface mannose receptor and Fizz1 mRNA, both M2 markers. Global gene expression analysis further revealed activation of pro-inflammatory, pro-atherosclerotic pathways. Analysis of tumor-infiltrating lymphocytes (TILs) demonstrated markedly increased activated CD8 T cell numbers, and CD8 T cell depletion obviated the inhibitory effect of myeloid Klf4 deletion on prostate cancer growth. These findings suggest that reducing expression or activity of the Klf4 transcription factor in tumor myeloid cells may contribute to prostate cancer therapy.
[Mh] Termos MeSH primário: Fatores de Transcrição Kruppel-Like/deficiência
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
[Mh] Termos MeSH secundário: Animais
Aterosclerose/etiologia
Proteína beta Intensificadora de Ligação a CCAAT/deficiência
Proteína beta Intensificadora de Ligação a CCAAT/genética
Antígeno CD11c/metabolismo
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Linhagem Celular Tumoral
Fatores de Transcrição Kruppel-Like/genética
Lectinas Tipo C/metabolismo
Linfócitos do Interstício Tumoral
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/patologia
Masculino
Lectinas de Ligação a Manose/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células Mieloides/imunologia
Células Mieloides/metabolismo
Células Mieloides/patologia
Neoplasias da Próstata/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
Receptores de Superfície Celular/metabolismo
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Protein-beta); 0 (CD11c Antigen); 0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (RNA, Messenger); 0 (RNA, Neoplasm); 0 (Receptors, Cell Surface); 0 (mannose receptor)
[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:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191188


  2 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468968
[Au] Autor:Ocaña-Morgner C; Sales S; Rothe M; Shevchenko A; Jessberger R
[Ad] Endereço:Institute of Physiological Chemistry, Faculty of Medicine Carl Gustav Carus, Dresden University of Technology, Dresden 01307, Germany; and carlos.ocana-morgner@mailbox.tu-dresden.de rolf.jessberger@mailbox.tu-dresden.de.
[Ti] Título:Tolerogenic versus Immunogenic Lipidomic Profiles of CD11c Immune Cells and Control of Immunogenic Dendritic Cell Ceramide Dynamics.
[So] Source:J Immunol;198(11):4360-4372, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lipids affect the membrane properties determining essential biological processes. Earlier studies have suggested a role of switch-activated protein 70 (SWAP-70) in lipid raft formation of dendritic cells. We used lipidomics combined with genetic and biochemical assays to analyze the role of SWAP-70 in lipid dynamics. TLR activation using LPS as a ligand represented a pathogenic immunogenic stimulus, physical disruption of cell-cell contacts a tolerogenic stimulus. Physical disruption, but not LPS, caused an increase of phosphatidylcholine ether and cholesteryl esters in CD11c immune cells. An increase of ceramide (Cer) was a hallmark for LPS activation. SWAP-70 was required for regulating the increase and localization of Cers in the cell membrane. SWAP-70 controls Cer accumulation through the regulation of pH-dependent acid-sphingomyelinase activity and of RhoA-dependent transport of endosomal contents to the plasma membrane. Poor accumulation of Cers in cells caused decreased apoptosis. This shows that two different pathways of activation, immunogenic and tolerogenic, induce different changes in the lipid composition of cultured CD11c cells, and highlights the important role of SWAP-70 in Cer dynamics in dendritic cells.
[Mh] Termos MeSH primário: Antígeno CD11c/imunologia
Ceramidas/metabolismo
Proteínas de Ligação a DNA/metabolismo
Células Dendríticas/imunologia
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Tolerância Imunológica
Lipídeos/imunologia
Antígenos de Histocompatibilidade Menor/metabolismo
Proteínas Nucleares/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Linhagem Celular
Células Cultivadas
Ceramidas/imunologia
Ésteres do Colesterol/genética
Ésteres do Colesterol/imunologia
Meios de Cultura/química
Citocinas/biossíntese
Citocinas/imunologia
Proteínas de Ligação a DNA/genética
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Fatores de Troca do Nucleotídeo Guanina/genética
Lipídeos/análise
Lipopolissacarídeos/imunologia
Camundongos
Antígenos de Histocompatibilidade Menor/genética
Proteínas Nucleares/genética
Esfingomielina Fosfodiesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (Ceramides); 0 (Cholesterol Esters); 0 (Culture Media); 0 (Cytokines); 0 (DNA-Binding Proteins); 0 (Guanine Nucleotide Exchange Factors); 0 (Lipids); 0 (Lipopolysaccharides); 0 (Minor Histocompatibility Antigens); 0 (Nuclear Proteins); 0 (Swap70 protein, mouse); EC 3.1.4.12 (Sphingomyelin Phosphodiesterase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601928


  3 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28457482
[Au] Autor:Frasca D; Diaz A; Romero M; D'Eramo F; Blomberg BB
[Ad] Endereço:Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101, USA. Electronic address: dfrasca@med.miami.edu.
[Ti] Título:Aging effects on T-bet expression in human B cell subsets.
[So] Source:Cell Immunol;321:68-73, 2017 Nov.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In order to compare human and mouse B cell subset markers, we evaluated T-bet expression in human B cell subsets from individuals of different ages. We found T-bet expressed in unstimulated memory more than naïve B cells, and more in young individuals. TLR7 stimulation up-regulated T-bet in all B cell subsets from young and elderly individuals, and more in the elderly. By fold-increase the best effect was seen in subsets of the elderly and especially in those that undergo class switch (naïve and IgM). We also evaluated CD11c expression, as T-bet+CD11c+ B cells are expanded in healthy elderly individuals and also in patients with autoimmunity. Similar to T-bet, CD11c expression was higher in memory than in naïve B cells, but no differences were observed between young and elderly individuals. After TLR7 stimulation, CD11c increases in all B cell subsets (especially in naïve and IgM) from the elderly.
[Mh] Termos MeSH primário: Envelhecimento
Subpopulações de Linfócitos B/metabolismo
Linfócitos B/metabolismo
Proteínas com Domínio T-Box/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígeno CD11c/metabolismo
Células Cultivadas
Feminino
Citometria de Fluxo
Seres Humanos
Imidazóis/farmacologia
Masculino
Meia-Idade
Receptor 7 Toll-Like/agonistas
Receptor 7 Toll-Like/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (Imidazoles); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 0 (TLR7 protein, human); 0 (Toll-Like Receptor 7); V3DMU7PVXF (resiquimod)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  4 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28963930
[Au] Autor:Li Y; Yu Q; Zhao W; Zhang J; Liu W; Huang M; Zeng X
[Ad] Endereço:Department of Respiratory & Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu 210029, China.
[Ti] Título:Oligomeric proanthocyanidins attenuate airway inflammation in asthma by inhibiting dendritic cells maturation.
[So] Source:Mol Immunol;91:209-217, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To date, although a promising anti-inflammatory activity of oligomeric proanthocyanidins (OPCs) has been observed in asthma, the mechanism responsible for these immunomodulatory properties remains obscure. Dendritic cells (DCs) that reside in the airway have been widely perceived as an important contributor to asthma. Our study was to demonstrate OPCs' effects on maturation and immunoregulation of pulmonary CD11c dendritic cells (DCs). BALB/c mice were exposed to ovalbumin (OVA) to induce murine model of asthma. In addition, pulmonary DCs and bone marrow-derived DCs (BMDCs) cultures were used to evaluate impacts of OPCs on DCs function. The results obtained here indicated that OPCs treatment dramatically reduced airway inflammation, such as the infiltration of inflammatory cells and the levels of allergen-specific serum IgE and Th2 cytokines. The expression of co-stimulatory molecules especially CD86 distributed on pulmonary DCs and bone marrow-derived DCs (BMDCs) also markedly declined. The phosphorylation of cAMP responsive element-binding protein (CREB) was significantly inhibited while no changes were observed in the expression of cAMP responsive element modulator (CREM). By transferring BMDCs into the airways of naïve mice, we found that OPCs-treated DCs (DC+OVA+OPC) were much less potent in promoting CD4 T cells proliferation than OVA-pulsed DCs (DC+OVA), followed by the ameliorated eosinophilic inflammation in airway. Our findings tailor a novel profile of OPCs in the regulation of DCs function, shedding new light on the therapeutic potential of OPCs in asthma management.
[Mh] Termos MeSH primário: Asma/imunologia
Células Dendríticas/imunologia
Pulmão/imunologia
Proantocianidinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Asma/induzido quimicamente
Asma/patologia
Antígeno B7-2/imunologia
Antígeno CD11c/imunologia
Proteína de Ligação a CREB/imunologia
Proliferação Celular/efeitos dos fármacos
Citocinas/imunologia
Células Dendríticas/patologia
Feminino
Imunoglobulina E/imunologia
Inflamação/induzido quimicamente
Inflamação/imunologia
Inflamação/patologia
Pulmão/patologia
Camundongos
Camundongos Endogâmicos BALB C
Fosforilação/efeitos dos fármacos
Fosforilação/imunologia
Células Th2/imunologia
Células Th2/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (CD11c Antigen); 0 (Cd86 protein, mouse); 0 (Cytokines); 0 (Proanthocyanidins); 37341-29-0 (Immunoglobulin E); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (Crebbp protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE


  5 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28864471
[Au] Autor:Smith T; Lin X; Mello M; Marquardt K; Cheung J; Lu B; Sherman LA; Verdeil G
[Ad] Endereço:Department of Immunology and Microbiology, Scripps Research Institute, La Jolla, CA 92037.
[Ti] Título:Peripheral Deletion of CD8 T Cells Requires p38 MAPK in Cross-Presenting Dendritic Cells.
[So] Source:J Immunol;199(8):2713-2720, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral tolerance mechanisms exist to prevent autoimmune destruction by self-reactive T cells that escape thymic deletion. Dominant tolerance imposed by CD4 Foxp3 T regulatory cells can actively control autoaggressive T cell responses. Tolerance mechanisms that act endogenous to the T cell also exist. These mechanisms include T cell inactivation (anergy) and deletion. A major difference between anergic T cells and T cells undergoing peripheral deletion is the capacity of the latter to still signal through MAPKs upon TCR stimulation, suggesting these signals may be required for T deletion. In this study, we used several different models of CD8 T cell deletion to investigate the contribution of MAPK activation. Using chemical inhibitors, we established that inhibition of p38, but not ERK or JNK, rescue T cells from undergoing peripheral deletion both in vitro and in vivo. Using T cell-specific murine lines genetically altered in expression of p38α, and mice in which p38α was deleted only in CD11c-expressing cells, we surprisingly found that CD8 T cell-intrinsic p38α activation was not responsible for increased survival, but rather that inhibition of p38α in the Ag-presenting dendritic cells prevented CD8 T cell deletion.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/fisiologia
Deleção Clonal
Células Dendríticas/imunologia
Tolerância Periférica
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno CD11c/metabolismo
Linhagem Celular
Apresentação Cruzada
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T/metabolismo
Transdução de Sinais
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (Receptors, Antigen, T-Cell); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700427


  6 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28779023
[Au] Autor:Zaman TS; Arimochi H; Maruyama S; Ishifune C; Tsukumo SI; Kitamura A; Yasutomo K
[Ad] Endereço:Department of Immunology and Parasitology, Graduate School of Medicine, Tokushima University, Tokushima 770-8503, Japan.
[Ti] Título:Notch Balances Th17 and Induced Regulatory T Cell Functions in Dendritic Cells by Regulating Expression.
[So] Source:J Immunol;199(6):1989-1997, 2017 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DCs) are important for adaptive immune responses through the activation of T cells. The molecular interplay between DCs and T cells determines the magnitude of T cell responses or outcomes of functional differentiation of T cells. In this study, we demonstrated that DCs in mice that are deficient in CD11c cells (Rbpj mice) promoted the differentiation of IL-17A-producing Th17 cells. -deficient DCs expressed little Aldh1a2 protein that is required for generating retinoic acid. Those DCs exhibited a reduced ability for differentiating regulatory T cells induced by TGF-ß. Rbpj protein directly regulated transcription by binding to its promoter region. The overexpression of in Rbpj-deficient DCs negated their Th17-promoting ability. Transfer of naive CD4 T cells into -deficient Rbpj mice enhanced colitis with increased Th17 and reduced induced regulatory T cells (iTreg) compared with control -deficient mice. The cotransfer of iTreg and naive CD4 T cells into -deficient Rbpj mice improved colitis compared with transfer of naive CD4 T cell alone. Furthermore, cotransfer of DCs from Rbpj mice that overexpressed or Notch-stimulated DCs together with naive CD4 T cells into Rbpj -deficient mice led to reduced colitis with increased iTreg numbers. Therefore, our studies identify Notch signaling in DCs as a crucial balancer of Th17/iTreg, which depends on the direct regulation of transcription in DCs.
[Mh] Termos MeSH primário: Colite/imunologia
Células Dendríticas/imunologia
Retinal Desidrogenase/metabolismo
Linfócitos T Reguladores/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Animais
Antígeno CD11c/metabolismo
Diferenciação Celular
Células Cultivadas
Regulação da Expressão Gênica
Genes RAG-1
Seres Humanos
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/genética
Interleucina-17/metabolismo
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores Notch/metabolismo
Retinal Desidrogenase/genética
Linfócitos T Reguladores/transplante
Tretinoína/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (Immunoglobulin J Recombination Signal Sequence-Binding Protein); 0 (Interleukin-17); 0 (Rbpj protein, mouse); 0 (Receptors, Notch); 5688UTC01R (Tretinoin); EC 1.2.1.36 (ALDH1A2 protein, human); 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:AIM; IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700645


  7 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28722110
[Au] Autor:Liao X; Ren J; Reihl A; Pirapakaran T; Sreekumar B; Cecere TE; Reilly CM; Luo XM
[Ad] Endereço:Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
[Ti] Título:Renal-infiltrating CD11c cells are pathogenic in murine lupus nephritis through promoting CD4 T cell responses.
[So] Source:Clin Exp Immunol;190(2):187-200, 2017 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40-60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus-prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus-prone mouse models, we showed the pathogenic role of a kidney-infiltrating CD11c myeloid cell population in LN. These CD11c cells accumulated in the kidneys of lupus-prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C) mature monocytes. The cytokine/chemokine profile of these renal-infiltrating CD11c cells suggests their roles in promoting LN, which was confirmed further in a loss-of-function in-vivo study by using an antibody-drug conjugate (ADC) strategy targeting CX CR1, a chemokine receptor expressed highly on these CD11c cells. However, CX CR1 was dispensable for the homing of CD11c cells into lupus nephritic kidneys. Finally, we found that these CD11c cells co-localized with infiltrating T cells in the kidney. Using an ex- vivo co-culture system, we showed that renal-infiltrating CD11c cells promoted the survival, proliferation and interferon-γ production of renal-infiltrating CD4 T cells, suggesting a T cell-dependent mechanism by which these CD11c cells promote LN. Together, our results identify a pathogenic kidney-infiltrating CD11c cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN.
[Mh] Termos MeSH primário: Antígeno CD11c/imunologia
Linfócitos T CD4-Positivos/imunologia
Rim/imunologia
Nefrite Lúpica/imunologia
Células Mieloides/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/imunologia
Receptor 1 de Quimiocina CX3C
Movimento Celular
Quimiocinas/imunologia
Técnicas de Cocultura
Citocinas/imunologia
Células Dendríticas/imunologia
Modelos Animais de Doenças
Interferon gama/biossíntese
Interferon gama/imunologia
Rim/patologia
Nefrite Lúpica/fisiopatologia
Camundongos
Células Mieloides/imunologia
Receptores de Quimiocinas/genética
Receptores de Quimiocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (CD11c Antigen); 0 (CX3C Chemokine Receptor 1); 0 (Chemokines); 0 (Cx3cr1 protein, mouse); 0 (Cytokines); 0 (Ly6 protein, mouse); 0 (Receptors, Chemokine); 82115-62-6 (Interferon-gamma)
[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:170720
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13017


  8 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28698173
[Au] Autor:Seneviratne AN; Edsfeldt A; Cole JE; Kassiteridi C; Swart M; Park I; Green P; Khoyratty T; Saliba D; Goddard ME; Sansom SN; Goncalves I; Krams R; Udalova IA; Monaco C
[Ad] Endereço:From Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, United Kingdom (A.N.S., A.E., J.E.C., C.K., M.S., I.P., P.G., T.K., D.S., M.E.G., S.N.S., I.A.U., C.M.); Department of Bioengineering, Imperial College London
[Ti] Título:Interferon Regulatory Factor 5 Controls Necrotic Core Formation in Atherosclerotic Lesions by Impairing Efferocytosis.
[So] Source:Circulation;136(12):1140-1154, 2017 Sep 19.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Myeloid cells are central to atherosclerotic lesion development and vulnerable plaque formation. Impaired ability of arterial phagocytes to uptake apoptotic cells (efferocytosis) promotes lesion growth and establishment of a necrotic core. The transcription factor interferon regulatory factor (IRF)-5 is an important modulator of myeloid function and programming. We sought to investigate whether IRF5 affects the formation and phenotype of atherosclerotic lesions. METHODS: We investigated the role of IRF5 in atherosclerosis in 2 complementary models. First, atherosclerotic lesion development in hyperlipidemic apolipoprotein E-deficient (ApoE ) mice and ApoE mice with a genetic deletion of IRF5 (ApoE Irf5 ) was compared and then lesion development was assessed in a model of shear stress-modulated vulnerable plaque formation. RESULTS: Both lesion and necrotic core size were significantly reduced in ApoE Irf5 mice compared with IRF5-competent ApoE mice. Necrotic core size was also reduced in the model of shear stress-modulated vulnerable plaque formation. A significant loss of CD11c macrophages was evident in ApoE Irf5 mice in the aorta, draining lymph nodes, and bone marrow cell cultures, indicating that IRF5 maintains CD11c macrophages in atherosclerosis. Moreover, we revealed that the CD11c gene is a direct target of IRF5 in macrophages. In the absence of IRF5, CD11c macrophages displayed a significant increase in expression of the efferocytosis-regulating integrin-ß3 and its ligand milk fat globule-epidermal growth factor 8 protein and enhanced efferocytosis in vitro and in situ. CONCLUSIONS: IRF5 is detrimental in atherosclerosis by promoting the maintenance of proinflammatory CD11c macrophages within lesions and controlling the expansion of the necrotic core by impairing efferocytosis.
[Mh] Termos MeSH primário: Aterosclerose/patologia
Fatores Reguladores de Interferon/metabolismo
[Mh] Termos MeSH secundário: Animais
Aorta/metabolismo
Aorta/patologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Aterosclerose/metabolismo
Células da Medula Óssea/citologia
Células da Medula Óssea/metabolismo
Antígeno CD11c/genética
Antígeno CD11c/metabolismo
Células Cultivadas
Imuno-Histoquímica
Integrina beta3/metabolismo
Fatores Reguladores de Interferon/deficiência
Fatores Reguladores de Interferon/genética
Linfonodos/citologia
Macrófagos/citologia
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Necrose
Fagocitose
Resistência ao Cisalhamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (CD11c Antigen); 0 (Integrin beta3); 0 (Interferon Regulatory Factors); 0 (Irf5 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.117.027844


  9 / 1343 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28646573
[Au] Autor:Pennell LM; Fish EN
[Ad] Endereço:Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
[Ti] Título:Interferon-ß regulates dendritic cell activation and migration in experimental autoimmune encephalomyelitis.
[So] Source:Immunology;152(3):439-450, 2017 Nov.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CD11c dendritic cells (DCs) exert a critical role as antigen-presenting cells in regulating pathogenic T cells in multiple sclerosis (MS). To determine whether the therapeutic benefit of interferon-ß (IFN-ß) treatment for MS is in part influenced by IFN regulation of DC function, we examined the immunophenotype of DCs derived from IFN-ß and IFN-ß mice using a myelin oligodendrocyte glycoprotein (MOG) peptide-induced mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Our earlier work identified that IFN-ß mice exhibit earlier onset and more rapid progression of neurological impairment compared with IFN-ß mice. In this study we show that lipopolysaccharide-/MOG peptide-stimulated IFN-ß DCs secrete cytokines associated with pathological T helper type 17 rather than regulatory T-cell polarization and exhibit increased CD80 and MHCII expression when compared with stimulated IFN-ß DCs. IFN-ß DCs from mice immunized to develop EAE induce greater proliferation of MOG-transgenic CD4 T cells and promote interleukin-17 production by these T cells. Adoptive transfer of MOG peptide-primed IFN-ß DCs into IFN-ß and IFN-ß mice immunized to develop EAE resulted in their rapid migration into the central nervous system of recipient mice, before onset of disease, which we attribute to failed signal transducer and activator of transcription 1-mediated inhibition of CCR7. Taken together, our data support immunoregulatory roles for IFN-ß in the activation and migration of DCs during EAE.
[Mh] Termos MeSH primário: Quimiotaxia
Células Dendríticas/metabolismo
Encefalomielite Autoimune Experimental/metabolismo
Interferon beta/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Antígeno CD11c/imunologia
Antígeno CD11c/metabolismo
Linhagem da Célula
Plasticidade Celular
Proliferação Celular
Células Cultivadas
Técnicas de Cocultura
Células Dendríticas/imunologia
Células Dendríticas/transplante
Encefalomielite Autoimune Experimental/genética
Encefalomielite Autoimune Experimental/imunologia
Predisposição Genética para Doença
Interferon beta/deficiência
Interferon beta/genética
Interferon beta/imunologia
Lipopolissacarídeos/imunologia
Ativação Linfocitária
Camundongos Endogâmicos C57BL
Camundongos Knockout
Glicoproteína Mielina-Oligodendrócito/imunologia
Fragmentos de Peptídeos/imunologia
Fenótipo
Receptores CCR7/imunologia
Receptores CCR7/metabolismo
Fator de Transcrição STAT1/imunologia
Fator de Transcrição STAT1/metabolismo
Células Th17/imunologia
Células Th17/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (Ccr7 protein, mouse); 0 (Lipopolysaccharides); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (Receptors, CCR7); 0 (STAT1 Transcription Factor); 0 (Stat1 protein, mouse); 0 (myelin oligodendrocyte glycoprotein (35-55)); 77238-31-4 (Interferon-beta)
[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:170625
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12781


  10 / 1343 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28603911
[Au] Autor:Umit EG; Baysal M; Durmus Y; Demir AM
[Ad] Endereço:Department of Hematology, Faculty of Medicine Trakya University, Edirne, Turkey.
[Ti] Título:CD11c expression in chronic lymphocytic leukemia revisited, related with complications and survival.
[So] Source:Int J Lab Hematol;39(5):552-556, 2017 Oct.
[Is] ISSN:1751-553X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Chronic lymphocytic leukemia (CLL) is a disorder of mature but dysfunctional monoclonal B cells. Microenvironment, antigenic stimulation and genetical mutations are demonstrated in etiopathogenesis. We aimed to evaluate the expression of CD11c in patients with CLL and its possible clinical significance. METHODS: Data of 259 patients with CLL between 2010 and 2016 in Trakya University Faculty of Medicine, including age at diagnosis, sex, whole blood count, stage, percentage of CLL cells in bone marrow, line of treatments, development of Richter's transformation and secondary tumors, autoimmune complications, IgG level, prognostic cytogenetic analysis, and length of survival were recorded from files. RESULTS: 151 patients were male (58.3%) and 108 were male (41.7%). Mean age was 70 (21-92) years. CD11c was observed to be positive (>%20) in 103 patients (39.8%). Development of Richter's transformation, secondary tumors and ITP was significantly frequent in patients with CD11c positivity (P values .000, .003, .000 respectively). Also, IgG levels were significantly lower in this group (P = .000). Hemoglobin level, RAI stage and bone marrow CLL infiltration percentage were statistically related with CD11c (P values .036, .037, .000 respectively). Finally, CD11c was statistically related (in positive group 70 months, negative group 79 months, P = .001). CONCLUSION: CD11c, expressed not only in Hairy cell leukemia but also in dendritic cells, macrophages and monocytes is a differentiation marker for inflammation. Prolonged inflammation in the microenvironment of CLL cells may cause a susceptibility to autoimmune disorders and secondary tumors in CLL, in this way, an increase in mortality.
[Mh] Termos MeSH primário: Antígeno CD11c/genética
Expressão Gênica
Leucemia Linfocítica Crônica de Células B/genética
Leucemia Linfocítica Crônica de Células B/mortalidade
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Doenças Autoimunes/etiologia
Biomarcadores Tumorais
Medula Óssea/patologia
Aberrações Cromossômicas
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Leucemia Linfocítica Crônica de Células B/complicações
Masculino
Meia-Idade
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CD11c 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:170613
[St] Status:MEDLINE
[do] DOI:10.1111/ijlh.12695



página 1 de 135 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