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  1 / 2038 MEDLINE  
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[PMID]:28696253
[Au] Autor:Sitrin J; Suto E; Wuster A; Eastham-Anderson J; Kim JM; Austin CD; Lee WP; Behrens TW
[Ad] Endereço:Department of Human Genetics, Genentech, Inc., South San Francisco, CA 94080; sitrinjr@gmail.com.
[Ti] Título:The Ox40/Ox40 Ligand Pathway Promotes Pathogenic Th Cell Responses, Plasmablast Accumulation, and Lupus Nephritis in NZB/W F1 Mice.
[So] Source:J Immunol;199(4):1238-1249, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ox40 ligand (Ox40L) locus genetic variants are associated with the risk for systemic lupus erythematosus (SLE); however, it is unclear how Ox40L contributes to SLE pathogenesis. In this study, we evaluated the contribution of Ox40L and its cognate receptor, Ox40, using in vivo agonist and antagonist approaches in the NZB × NZW (NZB/W) F1 mouse model of SLE. Ox40 was highly expressed on several CD4 Th cell subsets in the spleen and kidney of diseased mice, and expression correlated with disease severity. Treatment of aged NZB/W F1 mice with agonist anti-Ox40 mAbs potently exacerbated renal disease, which was accompanied by activation of kidney-infiltrating T cells and cytokine production. The agonist mAbs also induced activation and inflammatory gene expression in splenic CD4 T cells, including IFN-regulated genes, increased the number of follicular helper T cells and plasmablasts in the spleen, and led to elevated levels of serum IgM and enhanced renal glomerular IgM deposition. In a type I IFN-accelerated lupus model, treatment with an antagonist Ox40:Fc fusion protein significantly delayed the onset of severe proteinuria and improved survival. These data support the hypothesis that the Ox40/Ox40L pathway drives cellular and humoral autoimmune responses during lupus nephritis in NZB/W F1 mice and emphasize the potential clinical value of targeting this pathway in human lupus.
[Mh] Termos MeSH primário: Nefrite Lúpica/imunologia
Glicoproteínas de Membrana/metabolismo
Plasmócitos/imunologia
Receptores OX40/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Antinucleares/imunologia
Anticorpos Monoclonais/imunologia
Autoimunidade
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Modelos Animais de Doenças
Feminino
Seres Humanos
Rim/imunologia
Rim/patologia
Glomérulos Renais/imunologia
Glomérulos Renais/patologia
Nefrite Lúpica/fisiopatologia
Camundongos
Camundongos Endogâmicos NZB
Proteinúria/imunologia
Transdução de Sinais
Linfócitos T Auxiliares-Indutores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Antibodies, Monoclonal); 0 (Membrane Glycoproteins); 0 (Receptors, OX40); 0 (Tnfrsf4 protein, mouse); 0 (Tnfsf4 protein, mouse); 0 (Tumor Necrosis Factors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700608


  2 / 2038 MEDLINE  
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[PMID]:28639899
[Au] Autor:Hu G; Zeng W; Xia Y
[Ad] Endereço:Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
[Ti] Título:TWEAK/Fn14 signaling in tumors.
[So] Source:Tumour Biol;39(6):1010428317714624, 2017 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TWEAK (tumor necrosis factor-related weak inducer of apoptosis), a member of the tumor necrosis factor superfamily, acts on cells by binding to its only receptor named Fn14 (fibroblast growth factor-inducible 14). Their engagement activates a number of intracellular signal transduction cascades and consequently leads to cell death, proliferation, migration, or survival depending on the cellular contexts. Studies have indicated that the expression of TWEAK and Fn14 is upregulated in many solid tumors compared with healthy tissues. The activation of TWEAK/Fn14 signaling enhances the proliferation, invasion, and migration of tumor cells. Moreover, the angiogenesis, pro-inflammatory cytokine expression, and epithelial-mesenchymal transitions are promoted upon TWEAK/Fn14 activation. Currently, the tumor necrosis factor receptor-associated factor and nuclear factor kappa B signaling pathways are considered two main downstream pathways activated by TWEAK/Fn14 interaction. In view of these facts, some TWEAK- or Fn14-targeting agents are generated to inhibit the progression of tumors and have achieved initial success in clinical and pre-clinical trials. These agents include monoclonal antibodies, fusion proteins, immunotoxins, and nanoparticles. In addition, some relevant signaling pathways are studied to identify new potential therapeutic targets. Overall, these findings suggest that the TWEAK/Fn14 pathway is critical in the development of tumors, and targeting this signaling is a potential therapeutic approach in future tumor therapy.
[Mh] Termos MeSH primário: Neoplasias/genética
Receptores do Fator de Necrose Tumoral/genética
Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Movimento Celular/genética
Proliferação Celular/genética
Citocina TWEAK
Seres Humanos
Invasividade Neoplásica/genética
Neoplasias/patologia
Transdução de Sinais
Receptor de TWEAK
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokine TWEAK); 0 (Receptors, Tumor Necrosis Factor); 0 (TNFRSF12A protein, human); 0 (TNFSF12 protein, human); 0 (TWEAK Receptor); 0 (Tumor Necrosis Factors)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317714624


  3 / 2038 MEDLINE  
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[PMID]:28632765
[Au] Autor:Yan Z; Zhao J; Gan L; Zhang Y; Guo R; Cao X; Lau WB; Ma X; Wang Y
[Ad] Endereço:Department of Ophthalmology, The First Affiliated Hospital, Shanxi Medical University, Taiyuan, Shanxi, China.
[Ti] Título:CTRP3 is a novel biomarker for diabetic retinopathy and inhibits HGHL-induced VCAM-1 expression in an AMPK-dependent manner.
[So] Source:PLoS One;12(6):e0178253, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Diabetic retinopathy (DR) is a severe complication of chronic diabetes. The C1q/TNF-related protein family (CTRPs) has been demonstrated to exert protective effects against obesity and atherosclerosis in animal studies. Heretofore, the association between circulating CTRPs and DR patients has been unexplored. In the current study, we attempt to define this association, as well as the effect of CTRPs upon DR pathophysiology. DESIGN: The present investigation is a case control study that enrolled control subjects and type 2 diabetes mellitus (T2DM) patients diagnosed with DR. Serum CTRPs and sVACM-1 were determined by ELISA. RESULTS: Serum CTRP3 and CTRP5 levels were markedly decreased in patients with T2DM compared to controls (p<0.05) and inversely associated with T2DM. Furthermore, mutivariate regression and ROC analysis revealed CTRP3 deficiency, not CTRP5, was associated with proliferative diabetic retinopathy (PDR). Spearman's rank correlation assay demonstrated an inverse association between CTRP3 and sVCAM-1. Finally, exogenous CTRP3 administration attenuated high glucose high lipid (HGHL)-induced VCAM-1 production in an AMPK-dependent manner in cultured human retinal microvascular endothelial cells (HRMECs). CONCLUSION: CTRP3 may serve as a novel biomarker for DR severity. CTRP3 may represent a future novel therapeutic against DR, a common ocular complication of diabetes.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Biomarcadores/metabolismo
Retinopatia Diabética/diagnóstico
Glucose/efeitos adversos
Lipídeos/efeitos adversos
Fatores de Necrose Tumoral/metabolismo
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Células Cultivadas
Colágeno/metabolismo
Diabetes Mellitus Tipo 2/complicações
Retinopatia Diabética/etiologia
Retinopatia Diabética/metabolismo
Endotélio Vascular/citologia
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Vasos Retinianos/citologia
Vasos Retinianos/efeitos dos fármacos
Vasos Retinianos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (C1QTNF3 protein, human); 0 (C1QTNF5 protein, human); 0 (Lipids); 0 (Tumor Necrosis Factors); 0 (Vascular Cell Adhesion Molecule-1); 9007-34-5 (Collagen); EC 2.7.11.31 (AMP-Activated Protein Kinases); IY9XDZ35W2 (Glucose)
[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:170621
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178253


  4 / 2038 MEDLINE  
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[PMID]:28554843
[Au] Autor:Zhang X; Yin N; Guo A; Zhang Q; Zhang Y; Xu Y; Liu H; Tang B; Lai L
[Ad] Endereço:Center for Quantitative Biology, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.
[Ti] Título:NF-κB signaling and cell-fate decision induced by a fast-dissociating tumor necrosis factor mutant.
[So] Source:Biochem Biophys Res Commun;489(3):287-292, 2017 Jul 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor (TNF) is a pluripotent inflammatory cytokine that can induce both the pro-survival nuclear factor kappa B (NF-κB) pathway and the pro-apoptotic caspase pathway. Selectively activating only one of the two pathways remains challenging. We used TNF mutants with different receptor binding kinetics to study their effects on NF-κB signaling dynamics and cell apoptosis. A TNF mutant, R1antTNF, which binds to TNFR1 with increased association and dissociation rates, induced NF-κB signaling with shorter response time and first peak duration. The short nuclear stay of NF-κB led to biased activation of downstream genes, favoring the fast response ones. At the same time, R1antTNF retains pro-apoptotic activity. At 10 ng/ml, R1antTNF selectively activated the pro-apoptotic pathway rather than the pro-survival NF-κB pathway. Our study provides a new example for the emerging evidence that ligand-receptor binding kinetics play a key role in the selective activation of downstream pathways, which deserves more attention in future drug discovery and disease studies.
[Mh] Termos MeSH primário: Diferenciação Celular
NF-kappa B/metabolismo
Transdução de Sinais
Fatores de Necrose Tumoral/genética
Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Seres Humanos
Cinética
Ligação Proteica
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Tumor Necrosis Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE


  5 / 2038 MEDLINE  
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[PMID]:28551073
[Au] Autor:Nash P; Kirkham B; Okada M; Rahman P; Combe B; Burmester GR; Adams DH; Kerr L; Lee C; Shuler CL; Genovese M; SPIRIT-P2 Study Group
[Ad] Endereço:Department of Medicine, University of Queensland, Rheumatology Research Unit, Sunshine Coast, QLD, Australia. Electronic address: drpnash@tpg.com.au.
[Ti] Título:Ixekizumab for the treatment of patients with active psoriatic arthritis and an inadequate response to tumour necrosis factor inhibitors: results from the 24-week randomised, double-blind, placebo-controlled period of the SPIRIT-P2 phase 3 trial.
[So] Source:Lancet;389(10086):2317-2327, 2017 06 10.
[Is] ISSN:1474-547X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients who have had inadequate response to tumour necrosis factor inhibitors have fewer treatment options and are generally more treatment refractory to subsequent therapeutic interventions than previously untreated patients. We report the efficacy and safety of ixekizumab, a monoclonal antibody that selectively targets interleukin-17A, in patients with active psoriatic arthritis and previous inadequate response to tumour necrosis factor inhibitors. METHODS: In this double-blind, multicentre, randomised, placebo-controlled, phase 3 study (SPIRIT-P2), patients were recruited from 109 centres across ten countries in Asia, Australia, Europe, and North America. Patients were aged 18 years or older, had a confirmed diagnosis of psoriatic arthritis for at least 6 months, and had a previous inadequate response, distinguished by being refractory to therapy or had loss of efficacy, or were intolerant to tumour necrosis factor inhibitors. Patients were randomly assigned (1:1:1) by a computer-generated random sequence to receive a subcutaneous injection of 80 mg ixekizumab every 4 weeks or every 2 weeks after a 160 mg starting dose or placebo. The primary endpoint was the proportion of patients who attained at least 20% improvement in the American College of Rheumatology response criteria (ACR-20) at week 24. This study is registered with ClinicalTrials.gov, number NCT02349295. FINDINGS: Between March 3, 2015, to March 22, 2016, 363 patients were randomly assigned to placebo (n=118), ixekizumab every 4 weeks (n=122), or ixekizumab every 2 weeks (n=123). At week 24, a higher proportion of patients attained ACR-20 with ixekizumab every 4 weeks (65 [53%] patients; effect size vs placebo 33·8% [95% CI 22·4-45·2]; p<0·0001) and ixekizumab every 2 weeks (59 [48%] patients; 28.5% [17·1-39.8]; p<0·0001) than did patients with placebo (23 [20%] patients). Up to week 24, serious adverse events were reported in three (3%) patients with ixekizumab every 4 weeks, eight (7%) with ixekizumab every 2 weeks, and four (3%) with placebo; no deaths were reported. Infections were reported in 47 (39%) patients with ixekizumab every 4 weeks, 47 (38%) with ixekizumab every 2 weeks, and 35 (30%) with placebo. Three (2%) serious infections, all in patients in the ixekizumab every 2 weeks group, were reported. INTERPRETATION: Both the 2-week and 4-week ixekizumab dosing regimens improved the signs and symptoms of patients with active psoriatic arthritis and who had previously inadequate response to tumour necrosis factor inhibitors, with a safety profile consistent with previous studies investigating ixekizumab. FUNDING: Eli Lilly and Company.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Artrite Psoriásica/tratamento farmacológico
Fármacos Dermatológicos/uso terapêutico
Fatores de Necrose Tumoral/uso terapêutico
[Mh] Termos MeSH secundário: Método Duplo-Cego
Feminino
Saúde Global
Seres Humanos
Masculino
Meia-Idade
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Dermatologic Agents); 0 (Tumor Necrosis Factors); BTY153760O (ixekizumab)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


  6 / 2038 MEDLINE  
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[PMID]:28503960
[Au] Autor:Desbois AC; Vallet H; Domont F; Comarmond C; Cacoub P; Saadoun D
[Ad] Endereço:a Inflammation-Immunopathology-Biotherapy Department (DHU i2B) , Sorbonne Universités, UPMC Univ Paris 06, UMR 7211 , Paris , France.
[Ti] Título:Management of severe complications in Behçet's disease with TNF inhibitors.
[So] Source:Expert Opin Biol Ther;17(7):853-859, 2017 Jul.
[Is] ISSN:1744-7682
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The efficacy of anti-TNFα agents has been recently evaluated in many studies in Behçet's disease (BD), particularly in ocular and life-threatening manifestations such as neurological and vascular disease. Areas covered: The following article aims to summarize the currently available efficacy and safety data of anti-TNFα agents in BD. Expert opinion: Most studies have shown dramatic and rapid efficacy with anti-TNFα agents on the main BD-associated issues including posterior uveitis, gastro-intestinal and neurological complications as well as major vessel disease. Experts in the field do recommend the use of anti-TNF agents (either infliximab or adalimumab) as a first-line therapy in severe posterior uveitis in BD and now use anti-TNFα treatment in BD-associated life threatening manifestations. However, data is mainly based on retrospective cohorts or open-label prospective studies. Controlled studies (versus conventional immunosuppressants such as azathioprine and cyclophosphamide) are warranted to properly evaluate their efficacy as first line therapeutic in life-threatening manifestations of BD.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Síndrome de Behçet/tratamento farmacológico
Fatores de Necrose Tumoral/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adalimumab/uso terapêutico
Anticorpos Monoclonais/imunologia
Antimetabólitos Antineoplásicos/uso terapêutico
Azatioprina/uso terapêutico
Síndrome de Behçet/metabolismo
Síndrome de Behçet/patologia
Seres Humanos
Infliximab/uso terapêutico
Fatores de Necrose Tumoral/imunologia
Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antimetabolites, Antineoplastic); 0 (Tumor Necrosis Factors); B72HH48FLU (Infliximab); FYS6T7F842 (Adalimumab); MRK240IY2L (Azathioprine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1080/14712598.2017.1328496


  7 / 2038 MEDLINE  
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[PMID]:28493549
[Au] Autor:Qu SY; He YL; Zhang J; Wu CG
[Ad] Endereço:Department of Pulmonary and Critical Care Medicine, Fourth Military Medical University, Xi'an, China.
[Ti] Título:Transcription factor RBP-J-mediated signalling regulates basophil immunoregulatory function in mouse asthma model.
[So] Source:Immunology;152(1):115-124, 2017 Sep.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Basophils (BA) play an important role in the promotion of aberrant T helper type 2 (Th2) immune responses in asthma. It is not only the effective cell, but also modulates the initiation of Th2 immune responses. We earlier demonstrated that Notch signalling regulates the biological function of BAin vitro. However, whether this pathway plays the same role in vivo is not clear. The purpose of the present study was to investigate the effect of Notch signalling on BA function in the regulation of allergic airway inflammation in a murine model of asthma. Bone marrow BA were prepared by bone marrow cell culture in the presence of recombinant interleukin-3 (rIL-3; 300 pg/ml) for 7 days, followed by isolation of the CD49b microbeads. The recombination signal binding protein J (RBP-J ) BA were co-cultured with T cells, and the supernatant and the T-cell subtypes were examined. The results indicated disruption of the capacity of BA for antigen presentation alongside an up-regulation of the immunoregulatory function. This was possibly due to the low expression of OX40L in the RBP-J BA. Basophils were adoptively transferred to ovalbumin-sensitized recipient mice, to establish an asthma model. Lung pathology, cytokine profiles of brobchoalveolar fluid, airway hyperactivity and the absolute number of Th1/Th2 cells in lungs were determined. Overall, our results indicate that the RBP-J-mediated Notch signalling is critical for BA-dependent immunoregulation. Deficiency of RBP-J influences the immunoregulatory functions of BA, which include activation of T cells and their differentiation into T helper cell subtypes. The Notch signalling pathway is a potential therapeutic target for BA-based immunotherapy against asthma.
[Mh] Termos MeSH primário: Asma/imunologia
Basófilos/imunologia
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/imunologia
Pulmão/imunologia
Transdução de Sinais
Células Th2/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Asma/genética
Asma/metabolismo
Basófilos/metabolismo
Basófilos/transplante
Diferenciação Celular
Células Cultivadas
Técnicas de Cocultura
Modelos Animais de Doenças
Feminino
Genótipo
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/genética
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/metabolismo
Pulmão/metabolismo
Ativação Linfocitária
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/imunologia
Glicoproteínas de Membrana/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Ovalbumina
Fenótipo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores Notch/genética
Receptores Notch/imunologia
Receptores Notch/metabolismo
Células Th1/imunologia
Células Th1/metabolismo
Células Th2/metabolismo
Fatores de Necrose Tumoral/genética
Fatores de Necrose Tumoral/imunologia
Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin J Recombination Signal Sequence-Binding Protein); 0 (Membrane Glycoproteins); 0 (RNA, Messenger); 0 (Rbpj protein, mouse); 0 (Receptors, Notch); 0 (Tnfsf4 protein, mouse); 0 (Tumor Necrosis Factors); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12753


  8 / 2038 MEDLINE  
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[PMID]:28411440
[Au] Autor:Wang A; Zhang F; Xu H; Xu M; Cao Y; Wang C; Xu Y; Su M; Zhang M; Zhuge Y
[Ad] Endereço:Department of Gastroenterology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, China.
[Ti] Título:TWEAK/Fn14 promotes pro-inflammatory cytokine secretion in hepatic stellate cells via NF-κB/STAT3 pathways.
[So] Source:Mol Immunol;87:67-75, 2017 Jul.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) have been associated with liver disease. Hepatic stellate cells (HSCs) play a critical role in the hepatic wound-healing response after liver injury, but there is little information available on the role of the TWEAK/Fn14 pathway in human HSCs. In this study, we explored the role of TWEAK/Fn14 in activated human HSCs. The LX-2 cells were treated with TWEAK, and the expression of pro-inflammatory cytokines was assayed by enzyme-linked immunosorbent assay (ELISA) and real-time PCR (RT-PCR). Western blotting and RT-PCR were performed to evaluate the expression of Fn14 after TWEAK stimulation. Total and phosphorylated of inhibitor-κB (I-κB), nuclear factor kappa B (NF-κB), Janus kinase 2 (JAK2), and signal transducers and activators of transcription 3 (STAT3) were examined by western blotting after TWEAK stimulation and small interfering RNA (siRNA) transfection. The result showed that TWEAK upregulated the expression of Fn14 and pro-inflammatory factors interleukin-8 (IL-8), interleukin-6 (IL-6), regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemotactic protein-1 (MCP-1). In LX-2 cells, the pro-inflammatory cytokine secretion was closely related to the activation of the NF-κB and STAT3 pathways. Furthermore, our research showed that STAT3 and NF-κB could interact with each other, which resulted in a significant increase of pro-inflammatory cytokine secretion. The activation of NF-κB and STAT3 signalling-dependent pro-inflammatory cytokine expression may be responsible for such a novel principle and new therapeutic targets in chronic liver disease.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Células Estreladas do Fígado/metabolismo
Inflamação/metabolismo
NF-kappa B/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Fator de Transcrição STAT3/metabolismo
Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Quimiocina CCL2/metabolismo
Citocina TWEAK
Seres Humanos
Interleucina-6/metabolismo
Interleucina-8/metabolismo
Janus Quinase 2/metabolismo
RNA Interferente Pequeno/genética
Transdução de Sinais/fisiologia
Receptor de TWEAK
Fator de Necrose Tumoral alfa/metabolismo
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Cytokine TWEAK); 0 (Cytokines); 0 (Interleukin-6); 0 (Interleukin-8); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Receptors, Tumor Necrosis Factor); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (TNFRSF12A protein, human); 0 (TNFSF12 protein, human); 0 (TWEAK Receptor); 0 (Tumor Necrosis Factor-alpha); 0 (Tumor Necrosis Factors); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[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:170416
[St] Status:MEDLINE


  9 / 2038 MEDLINE  
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[PMID]:28397744
[Au] Autor:Cheng Z; Limbu MH; Wang Z; Liu J; Liu L; Zhang X; Chen P; Liu B
[Ad] Endereço:Department of Pathology and Pathophysiology, Medical School, Southeast University, Dingjiaqiao 87, Gulou District, Nanjing 210009, China. 230159257@seu.edu.cn.
[Ti] Título:MMP-2 and 9 in Chronic Kidney Disease.
[So] Source:Int J Mol Sci;18(4), 2017 Apr 08.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Gelatinases are members of the matrix metalloproteinase (MMPs) family; they play an important role in the degradation of the extracellular matrix (ECM). This effect is also crucial in the development and progression of chronic kidney disease (CKD). Its expression, as well as its activity regulation are closely related to the cell signaling pathways, hypoxia and cell membrane structural change. Gelatinases also can affect the development and progression of CKD through the various interactions with tumor necrosis factors (TNFs), monocyte chemoattractant proteins (MCPs), growth factors (GFs), oxidative stress (OS), and so on. Currently, their non-proteolytic function is a hot topic of research, which may also be associated with the progression of CKD. Therefore, with the in-depth understanding about the function of gelatinases, we can have a more specific and accurate understanding of their role in the human body.
[Mh] Termos MeSH primário: Matriz Extracelular/metabolismo
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Insuficiência Renal Crônica/enzimologia
[Mh] Termos MeSH secundário: Progressão da Doença
Seres Humanos
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Proteínas Quimioatraentes de Monócitos/metabolismo
Ligação Proteica
Insuficiência Renal Crônica/metabolismo
Insuficiência Renal Crônica/patologia
Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Intercellular Signaling Peptides and Proteins); 0 (Monocyte Chemoattractant Proteins); 0 (Tumor Necrosis Factors); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE


  10 / 2038 MEDLINE  
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[PMID]:28377447
[Au] Autor:Anwar S; Karim MY
[Ad] Endereço:Department of Medicine, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
[Ti] Título:Update on systemic vasculitides.
[So] Source:J Clin Pathol;70(6):476-482, 2017 Jun.
[Is] ISSN:1472-4146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Management of systemic vasculitis has been revolutionised over the last decade with the introduction of targeted biological agents. With an increase in both the prevalence and the recognition of vasculitis as well as the high cost of these agents, it is important to ensure their most optimal utilisation. The goals of vasculitis therapy include the induction and maintenance of remissions, preventing relapses, reducing the toxicity of therapy with the aim of reducing morbidity and mortality as well as improving the quality of life of those afflicted. This review focuses on the recent advances in the diagnosis, surveillance and treatment of these conditions.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Fatores Biológicos/uso terapêutico
Vasculite Sistêmica/tratamento farmacológico
[Mh] Termos MeSH secundário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/imunologia
Anticorpos Anticitoplasma de Neutrófilos/fisiologia
Anticorpos Monoclonais Humanizados/uso terapêutico
Fator Ativador de Células B/metabolismo
Via Alternativa do Complemento/fisiologia
Consenso
Seres Humanos
Imunoglobulina G/metabolismo
Imunoglobulinas Intravenosas/uso terapêutico
Imunossupressores/uso terapêutico
Interleucina-5/imunologia
Glicoproteínas de Membrana Associadas ao Lisossomo/imunologia
Medicina de Precisão/métodos
Receptor da Anafilatoxina C5a/antagonistas & inibidores
Receptores Depuradores/imunologia
Rituximab/uso terapêutico
Vasculite Sistêmica/etiologia
Fatores de Necrose Tumoral/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antibodies, Antineutrophil Cytoplasmic); 0 (Antibodies, Monoclonal, Humanized); 0 (B-Cell Activating Factor); 0 (Biological Factors); 0 (Immunoglobulin G); 0 (Immunoglobulins, Intravenous); 0 (Immunosuppressive Agents); 0 (Interleukin-5); 0 (Lysosome-Associated Membrane Glycoproteins); 0 (Receptor, Anaphylatoxin C5a); 0 (Receptors, Scavenger); 0 (SCARB2 protein, human); 0 (Tumor Necrosis Factors); 4F4X42SYQ6 (Rituximab); 73B0K5S26A (belimumab); I031V2H011 (tocilizumab)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1136/jclinpath-2016-203875



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