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[PMID]:29248579
[Au] Autor:Girardelli M; Basaldella F; Paolera SD; Vuch J; Tommasini A; Martelossi S; Crovella S; Bianco AM
[Ad] Endereço:Institute for Maternal and Child Health - IRCCS "Burlo Garofolo", Via dell'istria 65, Trieste, Italy.
[Ti] Título:Genetic profile of patients with early onset inflammatory bowel disease.
[So] Source:Gene;645:18-29, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Inflammatory Bowel disease (IBD) is a widespread pathological condition with clinical heterogeneity and with different levels of severity. Although IBD usually occurs in young adults, onset in childhood and infancy are described in patients within the 10th and second year of age. By genome-wide association studies and meta-analysis, several genetic loci have been identified associated with an increased risk of developing IBD in Western populations with variants that may alter the normal mucosal immunity in the gastrointestinal tract. The clinical complexity and the heterogeneity of the IBD phenotype probably reflect the presence of genetic heterogeneity where different genes or combinations of them may be involved, together with environmental factors. We hypothesized that patients with early onset IBD could have either more severe genetic variants in genes associated with IBD or multiple variants in different genes. Under the multifactorial diseases is crucial to consider the small contribution of a single variant in all not only to other small variations in the same gene but also in different genes belonging to the same pathway. We performed direct gene sequencing looking for 94 variations in NOD2, ATG16L1, IL23R, IL10R, IL10 and XIAP genes previously shown as correlated with IBD both in multifactorial and in Mendelian models. All variants identified are known in literature as being associated with IBD except for three variants in the genes NOD2, IL10 and IL10RB that even though present in online databases have never been involved in association studies on IBD patients. Moreover, we coupled genetic variants identification with an accurate "in silico" analysis to verify their predictive impact on the protein structure and function. The in-silico prediction of these variants results as benign therefore even if they exhibit a very low frequency in control population being benign, they cannot be considered pathogenic as monogenic disease but fall within the multifactorial range. The variants identified in our study partially reflect the association data described in the literature but there are no significant differences with the onset of disease (VEO vs EO-IBD).
[Mh] Termos MeSH primário: Predisposição Genética para Doença/genética
Doenças Inflamatórias Intestinais/genética
Polimorfismo de Nucleotídeo Único
Análise de Sequência de DNA/métodos
[Mh] Termos MeSH secundário: Idade de Início
Proteínas Relacionadas à Autofagia/genética
Criança
Pré-Escolar
Simulação por Computador
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Lactente
Interleucina-10/genética
Masculino
Proteína Adaptadora de Sinalização NOD2/genética
Receptores de Interleucina/genética
Receptores de Interleucina-10/genética
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATG16L1 protein, human); 0 (Autophagy-Related Proteins); 0 (IL10 protein, human); 0 (IL23R protein, human); 0 (NOD2 protein, human); 0 (Nod2 Signaling Adaptor Protein); 0 (Receptors, Interleukin); 0 (Receptors, Interleukin-10); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:29190678
[Au] Autor:Stefan KL; Fink A; Surana NK; Kasper DL; Dasgupta S
[Ad] Endereço:Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America.
[Ti] Título:Type I interferon signaling restrains IL-10R+ colonic macrophages and dendritic cells and leads to more severe Salmonella colitis.
[So] Source:PLoS One;12(11):e0188600, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type I interferons (IFNα, IFNß) are key regulators of innate and adaptive immunity, modulating the severity of both viral and bacterial infections. While type I IFN signaling leads to improved outcomes in viral infections, its role in bacterial infections is more contextual and depends on the specific pathogen and route of infection. Given the limited evidence on whether type I IFN signaling affects enteric bacterial pathogens, we investigated the role of this signaling pathway in Salmonella enterica serovar Typhimurium (S. typhimurium)-induced colitis. Comparing mice deficient in IFNAR1- the common receptor for IFNα and IFNß- with wild-type mice, we found that type I IFN signaling leads to more rapid death, more severe colonic inflammation, higher serum levels of pro-inflammatory cytokines, and greater bacterial dissemination. Specific ablation of plasmacytoid dendritic cells (pDCs), which are prominent producers of type I IFNs in antiviral responses, did not alter survival after infection. This result established that pDCs do not play a major role in the pathogenesis of S. typhimurium colitis. Flow cytometric analysis of macrophages and conventional dendritic cells (cDCs) during active colitis demonstrated an increase in CD11c- macrophages and CD103+ cDCs in the colon of Ifnar1-/- animals. Interestingly, cells expressing the anti-inflammatory cytokine receptor IL-10R are more abundant within these subsets in Ifnar1-/- than in wild-type mice. Moreover, blockade of IL-10R in Ifnar1-/- mice increased their susceptibility to S. typhimurium colitis, suggesting that altered numbers of these immunoregulatory cells may underlie the difference in disease severity. This cross-talk between type I IFN and IL-10R signaling pathways may represent a key host cellular mechanism to investigate further in order to unravel the balance between pathogenic inflammation and homeostasis of the colon. Taken together, our data clearly demonstrate that type I IFN signaling is pathogenic in S. typhimurium colitis.
[Mh] Termos MeSH primário: Colite/patologia
Células Dendríticas/metabolismo
Interferon Tipo I/metabolismo
Mucosa Intestinal/metabolismo
Macrófagos/metabolismo
Receptores de Interleucina-10/metabolismo
Infecções por Salmonella/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Colite/metabolismo
Colite/microbiologia
Citocinas/metabolismo
Mucosa Intestinal/citologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Infecções por Salmonella/microbiologia
Salmonella typhimurium/metabolismo
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interferon Type I); 0 (Receptors, Interleukin-10)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188600


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[PMID]:29016674
[Au] Autor:Wilbers RHP; van Raaij DR; Westerhof LB; Bakker J; Smant G; Schots A
[Ad] Endereço:Wageningen University and Research, Plant Sciences Group, Laboratory of Nematology, Wageningen, The Netherlands.
[Ti] Título:Re-evaluation of IL-10 signaling reveals novel insights on the contribution of the intracellular domain of the IL-10R2 chain.
[So] Source:PLoS One;12(10):e0186317, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin-10 (IL-10) is an anti-inflammatory cytokine that plays a key role in maintaining immune homeostasis. IL-10-mediated responses are triggered upon binding to a heterodimeric receptor complex consisting of IL-10 receptor (IL-10R)1 and IL-10R2. Engagement of the IL-10R complex activates the intracellular kinases Jak1 and Tyk2, but the exact roles of IL-10R2 and IL-10R2-associated signaling via Tyk2 remain unclear. To elucidate the contribution of IL-10R2 and its signaling to IL-10 activity, we re-evaluated IL-10-mediated responses on bone marrow-derived dendritic cells, macrophages and mast cells. By using bone marrow from IL-10R-/- mice it was revealed that IL-10-mediated responses depend on both IL-10R1 and IL-10R2 in all three cell types. On the contrary, bone marrow-derived cells from Tyk2-/- mice showed similar responses to IL-10 as wild-type cells, indicating that signaling via this IL-10R2-associated kinase only plays a limited role. Tyk2 was shown to control the amplitude of STAT3 activation and the up-regulation of downstream SOCS3 expression. SOCS3 up-regulation was found to be cell-type dependent and correlated with the lack of early suppression of LPS-induced TNF-α in dendritic cells. Further investigation of the IL-10R complex revealed that both the extracellular and intracellular domains of IL-10R2 influence the conformation of IL-10R1 and that both domains were required for transducing IL-10 signals. This observation highlights a novel role for the intracellular domain of IL-10R2 in the molecular mechanisms of IL-10R activation.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Interleucina-10/imunologia
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Interleucina-10/imunologia
Transdução de Sinais/imunologia
TYK2 Quinase/imunologia
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/citologia
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Clonagem Molecular
Células Dendríticas/citologia
Células Dendríticas/efeitos dos fármacos
Expressão Gênica
Regulação da Expressão Gênica
Interleucina-10/genética
Interleucina-10/farmacologia
Lipopolissacarídeos/farmacologia
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Mastócitos/citologia
Mastócitos/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Especificidade de Órgãos
Cultura Primária de Células
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Isoformas de Proteínas/deficiência
Isoformas de Proteínas/genética
Isoformas de Proteínas/imunologia
Receptores de Interleucina-10/deficiência
Receptores de Interleucina-10/genética
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/imunologia
Proteína 3 Supressora da Sinalização de Citocinas/genética
Proteína 3 Supressora da Sinalização de Citocinas/imunologia
TYK2 Quinase/deficiência
TYK2 Quinase/genética
Tabaco/genética
Tabaco/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Protein Isoforms); 0 (Receptors, Interleukin-10); 0 (Recombinant Proteins); 0 (STAT3 Transcription Factor); 0 (Socs3 protein, mouse); 0 (Stat3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); EC 2.7.10.2 (TYK2 Kinase); EC 2.7.10.2 (Tyk2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186317


  4 / 457 MEDLINE  
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[PMID]:28893958
[Au] Autor:Zheng L; Kelly CJ; Battista KD; Schaefer R; Lanis JM; Alexeev EE; Wang RX; Onyiah JC; Kominsky DJ; Colgan SP
[Ad] Endereço:Mucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045.
[Ti] Título:Microbial-Derived Butyrate Promotes Epithelial Barrier Function through IL-10 Receptor-Dependent Repression of Claudin-2.
[So] Source:J Immunol;199(8):2976-2984, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Commensal interactions between the enteric microbiota and distal intestine play important roles in regulating human health. Short-chain fatty acids (SCFAs), such as butyrate, produced through anaerobic microbial metabolism represent a major energy source for the host colonic epithelium and enhance epithelial barrier function through unclear mechanisms. Separate studies revealed that the epithelial anti-inflammatory IL-10 receptor α subunit (IL-10RA) is also important for barrier formation. Based on these findings, we examined if SCFAs promote epithelial barrier through IL-10RA-dependent mechanisms. Using human intestinal epithelial cells (IECs), we discovered that SCFAs, particularly butyrate, enhanced IEC barrier formation, induced IL-10RA mRNA, IL-10RA protein, and transactivation through activated Stat3 and HDAC inhibition. Loss and gain of IL-10RA expression directly correlates with IEC barrier formation and butyrate represses permeability-promoting claudin-2 tight-junction protein expression through an IL-10RA-dependent mechanism. Our findings provide a novel mechanism by which microbial-derived butyrate promotes barrier through IL-10RA-dependent repression of claudin-2.
[Mh] Termos MeSH primário: Bactérias Anaeróbias/fisiologia
Butiratos/metabolismo
Colo/patologia
Microbioma Gastrointestinal/imunologia
Mucosa Intestinal/fisiologia
Receptores de Interleucina-10/metabolismo
Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Butiratos/imunologia
Linhagem Celular
Células Cultivadas
Claudina-2/metabolismo
Regulação da Expressão Gênica
Histona Desacetilases/metabolismo
Seres Humanos
Mucosa Intestinal/microbiologia
Mucosa Intestinal/patologia
Receptores de Interleucina-10/genética
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Simbiose
Ativação Transcricional
Migração Transendotelial e Transepitelial
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Claudin-2); 0 (Receptors, Interleukin-10); 0 (STAT3 Transcription Factor); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700105


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[PMID]:28728914
[Au] Autor:Dudek MK; Michalak B; Wozniak M; Czerwinska ME; Filipek A; Granica S; Kiss AK
[Ad] Endereço:Centre of Molecular and Macromolecular Studies of Polish Academy of Sciences, Sienkiewicza 112, 90-363 Lodz, Poland.
[Ti] Título:Hydroxycinnamoyl derivatives and secoiridoid glycoside derivatives from Syringa vulgaris flowers and their effects on the pro-inflammatory responses of human neutrophils.
[So] Source:Fitoterapia;121:194-205, 2017 Sep.
[Is] ISSN:1873-6971
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Thirteen new compounds including caffeoyl-glucaric and p-coumaroyl-altraric acid derivatives, one monoterpenoid glucoside, four secoiridoid glycosides, and three hydroxycinnamoyl phenylpropanoid glycosides esterified with an oleoside 11-methyl ester along with fifteen known compounds were isolated from flowers of Syringa vulgaris L. (Oleaceae). Their structures were elucidated by high-resolution spectroscopic methods. The tested compounds were able to decrease the production of reactive oxygen species. Moreover, oleoechinacoside (13), demethylhydroxyoleonuezhenide (14), demethyloleonuezhenide (15), syringaoleoacteoside (25) and oleoacteoside (26) at the concentration of 50µM, moderately suppressed the LPS-stimulated release of pro-inflammatory chemokine IL-8 and TNF-α from human neutrophils. Moreover, oleonuezhenide (12), oleoside 11-methyl ester (16) and oleoacteoside (26) at the concentration of 50µM were able to induce the surface expression of interleukin 10 receptor, which is suppressed by the incubation of monocyte/macrophage cells with LPS.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Flores/química
Glicosídeos Iridoides/farmacologia
Neutrófilos/efeitos dos fármacos
Syringa/química
[Mh] Termos MeSH secundário: Anti-Inflamatórios/isolamento & purificação
Células Cultivadas
Glucosídeos/isolamento & purificação
Glucosídeos/farmacologia
Glicosídeos
Seres Humanos
Interleucina-8/metabolismo
Glicosídeos Iridoides/isolamento & purificação
Macrófagos/efeitos dos fármacos
Estrutura Molecular
Extratos Vegetais/química
Receptores de Interleucina-10/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Glucosides); 0 (Glycosides); 0 (IL8 protein, human); 0 (Interleukin-8); 0 (Iridoid Glycosides); 0 (Plant Extracts); 0 (Receptors, Interleukin-10); 0 (Tumor Necrosis Factor-alpha); 0 (oleoacteoside); 0 (oleoechinacoside)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


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[PMID]:28488547
[Au] Autor:Xi J; Xu M; Song Z; Li H; Xu S; Wang C; Song H; Bai J
[Ad] Endereço:1 Department of Geriatrics, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
[Ti] Título:Stimulatory role of interleukin 10 in CD8 T cells through STATs in gastric cancer.
[So] Source:Tumour Biol;39(5):1010428317706209, 2017 May.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD8 T cells are considered to be critical in tumor surveillance and elimination. Increased CD8 T cell frequency and function is associated with better prognosis in cancer patients. Interleukin 10 is a cytokine with controversial roles in CD8 T cell-mediated anti-tumor immunity. We therefore examined the interleukin 10 expression and consumption in CD8 T cells harvested from the peripheral blood and resected tumors of gastric cancer patients of stages II-IV. We found that the gastric cancer patients presented significantly elevated frequencies of interleukin 10-expressing cells in both CD4 and CD8 T cells compared to healthy controls. But distinctive from the interleukin 10-expressing CD4 T cells, which increased in frequency in advanced cancer, the interleukin 10-expressing CD8 T cells did not increase with cancer stage in the peripheral blood and actually decreased with cancer stage in resected tumor. Interleukin 10 and interleukin 10 receptor expression was also enriched in interferon gamma-expressing activated CD8 T cells. Compared to interleukin 10-nonexpressing CD8 T cells, interleukin 10 receptor-expressing CD8 T cells secreted significantly elevated interferon gamma levels. Treatment of anti-CD3/CD28-stimulated, purified CD8 T cells with interleukin 10 alone could significantly enhance CD8 T cell survival, an effect dependent on interleukin 10 receptor expression. Interleukin 10 also increased CD8 T cell proliferation synergistically with interferon gamma but not alone. Analysis of downstream signal transducer and activator of transcription molecules showed that interleukin 10 treatment significantly increased the phosphorylation of signal transducer and activator of transcription 3 and signal transducer and activator of transcription 1 to lesser extent. Together, these results demonstrate that interleukin 10 possessed stimulatory roles in activated CD8 T cells from gastric cancer patients.
[Mh] Termos MeSH primário: Interferon gama/genética
Interleucina-10/biossíntese
Receptores de Interleucina-10/genética
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD28/imunologia
Complexo CD3/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Proliferação Celular/genética
Feminino
Seres Humanos
Interferon gama/imunologia
Interleucina-10/genética
Masculino
Meia-Idade
Estadiamento de Neoplasias
Receptores de Interleucina-10/biossíntese
Fatores de Transcrição STAT/genética
Neoplasias Gástricas/imunologia
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD28 Antigens); 0 (CD3 Complex); 0 (IL10 protein, human); 0 (Receptors, Interleukin-10); 0 (STAT Transcription Factors); 130068-27-8 (Interleukin-10); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317706209


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[PMID]:28396319
[Au] Autor:Claser C; De Souza JB; Thorburn SG; Grau GE; Riley EM; Rénia L; Hafalla JCR
[Ad] Endereço:Laboratory of Pathogen Immunobiology, Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Biopolis, Singapore.
[Ti] Título:Host Resistance to Plasmodium-Induced Acute Immune Pathology Is Regulated by Interleukin-10 Receptor Signaling.
[So] Source:Infect Immun;85(6), 2017 Jun.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The resolution of malaria infection is dependent on a balance between proinflammatory and regulatory immune responses. While early effector T cell responses are required for limiting parasitemia, these responses need to be switched off by regulatory mechanisms in a timely manner to avoid immune-mediated tissue damage. Interleukin-10 receptor (IL-10R) signaling is considered to be a vital component of regulatory responses, although its role in host resistance to severe immune pathology during acute malaria infections is not fully understood. In this study, we have determined the contribution of IL-10R signaling to the regulation of immune responses during ANKA-induced experimental cerebral malaria (ECM). We show that antibody-mediated blockade of the IL-10R during ANKA infection in ECM-resistant BALB/c mice leads to amplified T cell activation, higher serum gamma interferon (IFN-γ) concentrations, enhanced intravascular accumulation of both parasitized red blood cells and CD8 T cells to the brain, and an increased incidence of ECM. Importantly, the pathogenic effects of IL-10R blockade during ANKA infection were reversible by depletion of T cells and neutralization of IFN-γ. Our findings underscore the importance of IL-10R signaling in preventing T-cell- and cytokine-mediated pathology during potentially lethal malaria infections.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Interferon gama/sangue
Malária Cerebral/imunologia
Plasmodium berghei/imunologia
Receptores de Interleucina-10/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Bloqueadores/administração & dosagem
Anticorpos Neutralizantes/administração & dosagem
Encéfalo/patologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Eritrócitos/efeitos dos fármacos
Eritrócitos/parasitologia
Feminino
Fígado/patologia
Ativação Linfocitária/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Parasitemia/imunologia
Receptores de Interleucina-10/antagonistas & inibidores
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (Antibodies, Neutralizing); 0 (Receptors, Interleukin-10); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE


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[PMID]:28329704
[Au] Autor:Mendoza JL; Schneider WM; Hoffmann HH; Vercauteren K; Jude KM; Xiong A; Moraga I; Horton TM; Glenn JS; de Jong YP; Rice CM; Garcia KC
[Ad] Endereço:Howard Hughes Medical Institute, Department of Molecular and Cellular Physiology and Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
[Ti] Título:The IFN-λ-IFN-λR1-IL-10Rß Complex Reveals Structural Features Underlying Type III IFN Functional Plasticity.
[So] Source:Immunity;46(3):379-392, 2017 Mar 21.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type III interferons (IFN-λs) signal through a heterodimeric receptor complex composed of the IFN-λR1 subunit, specific for IFN-λs, and interleukin-10Rß (IL-10Rß), which is shared by multiple cytokines in the IL-10 superfamily. Low affinity of IL-10Rß for cytokines has impeded efforts aimed at crystallizing cytokine-receptor complexes. We used yeast surface display to engineer a higher-affinity IFN-λ variant, H11, which enabled crystallization of the ternary complex. The structure revealed that IL-10Rß uses a network of tyrosine residues as hydrophobic anchor points to engage IL-10 family cytokines that present complementary hydrophobic binding patches, explaining its role as both a cross-reactive but cytokine-specific receptor. H11 elicited increased anti-proliferative and antiviral activities in vitro and in vivo. In contrast, engineered higher-affinity type I IFNs did not increase antiviral potency over wild-type type I IFNs. Our findings provide insight into cytokine recognition by the IL-10R family and highlight the plasticity of type III interferon signaling and its therapeutic potential.
[Mh] Termos MeSH primário: Interferons/imunologia
Receptores de Interferon/imunologia
Receptores de Interleucina-10/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cristalografia por Raios X
Citometria de Fluxo
Seres Humanos
Camundongos
Reação em Cadeia da Polimerase
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interferon); 0 (Receptors, Interleukin-10); 9008-11-1 (Interferons)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE


  9 / 457 MEDLINE  
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[PMID]:28225209
[Au] Autor:Ben Fredj N; Aissi M; Ben Selma W; Mahmoud I; Nefzi F; Frih-Ayed M; Boukadida J; Aouni M
[Ad] Endereço:Laboratory of Transmissible Diseases and Biological Active substances, LR99-ES27, Faculty of Pharmacy, University of Monastir, Monastir, Tunisia.
[Ti] Título:Association of the IL-10 receptor A536G (S138G) loss-of-function variant with multiple sclerosis in Tunisian patients.
[So] Source:APMIS;125(5):444-451, 2017 May.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Interleukin-10 (IL-10), a potent anti-inflammatory T-cell cytokine, has been shown to be a regulatory cytokine that is associated with disease remission in multiple sclerosis (MS) and exerts its activity through its cognate cell surface receptor complex, IL-10 receptor 1 (IL-10R1) and IL-10R2. The purpose of this study was to investigate the IL-10R1 S138G loss-of-function polymorphism (A536G: rs3135932) for possible influence on susceptibility and outcome of MS in Tunisian patients. A total of 103 Tunisian MS patients and 160 control subjects were studied. Genomic DNA samples were extracted from leukocytes and used to investigate S138G polymorphism in IL-10R1 gene by multiplex allele-specific polymerase chain reaction. Associations between G allele [odds ratio (OR) = 5.57; 95% confidence intervals (CI) = 3.26-9.54; p = 10 ], GG genotypes [OR = 10.41; 95% CI = 2.28-47.58; p = 0.0007] and AG genotype [OR = 4.14; 95% CI = 2.16-7.93; p = 0.000016] with the risk development of MS were found. In contrast, the AA genotype seemed to be associated with protection against MS [OR = 0.17; 95% CI = 0.09-0.30; p = 10 ]. No association was found between S138G SNP and clinical features or disease activity of MS patients. In conclusion, our results suggest that S138G loss-of-function polymorphism of the IL-10R1 may be important risk factor in increasing susceptibility to MS.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Esclerose Múltipla/epidemiologia
Esclerose Múltipla/genética
Mutação de Sentido Incorreto
Polimorfismo de Nucleotídeo Único
Receptores de Interleucina-10/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Feminino
Técnicas de Genotipagem
Seres Humanos
Masculino
Meia-Idade
Reação em Cadeia da Polimerase Multiplex
Tunísia/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-10)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12659


  10 / 457 MEDLINE  
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[PMID]:28003377
[Au] Autor:Brockmann L; Gagliani N; Steglich B; Giannou AD; Kempski J; Pelczar P; Geffken M; Mfarrej B; Huber F; Herkel J; Wan YY; Esplugues E; Battaglia M; Krebs CF; Flavell RA; Huber S
[Ad] Endereço:I.Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg 20246, Germany.
[Ti] Título:IL-10 Receptor Signaling Is Essential for TR1 Cell Function In Vivo.
[So] Source:J Immunol;198(3):1130-1141, 2017 Feb 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-10 is essential to maintain intestinal homeostasis. CD4 T regulatory type 1 (T 1) cells produce large amounts of this cytokine and are therefore currently being examined in clinical trials as T cell therapy in patients with inflammatory bowel disease. However, factors and molecular signals sustaining T 1 cell regulatory activity still need to be identified to optimize the efficiency and ensure the safety of these trials. We investigated the role of IL-10 signaling in mature T 1 cells in vivo. Double IL-10 Foxp3 reporter mice and transgenic mice with impairment in IL-10 receptor signaling were used to test the activity of T 1 cells in a murine inflammatory bowel disease model, a model that resembles the trials performed in humans. The molecular signaling was elucidated in vitro. Finally, we used human T 1 cells, currently employed for cell therapy, to confirm our results. We found that murine T 1 cells expressed functional IL-10Rα. T 1 cells with impaired IL-10 receptor signaling lost their regulatory activity in vivo. T 1 cells required IL-10 receptor signaling to activate p38 MAPK, thereby sustaining IL-10 production, which ultimately mediated their suppressive activity. Finally, we confirmed these data using human T 1 cells. In conclusion, T 1 cell regulatory activity is dependent on IL-10 receptor signaling. These data suggest that to optimize T 1 cell-based therapy, IL-10 receptor expression has to be taken into consideration.
[Mh] Termos MeSH primário: Receptores de Interleucina-10/fisiologia
Transdução de Sinais/fisiologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Interleucina-10/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Fosforilação
Fator de Transcrição STAT3/metabolismo
Células Th17/imunologia
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Interleukin-10); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 130068-27-8 (Interleukin-10); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601045



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