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[PMID]:28455312
[Au] Autor:Lopes N; Vachon H; Marie J; Irla M
[Ad] Endereço:Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille Cedex 09, France.
[Ti] Título:Administration of RANKL boosts thymic regeneration upon bone marrow transplantation.
[So] Source:EMBO Mol Med;9(6):835-851, 2017 Jun.
[Is] ISSN:1757-4684
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cytoablative treatments lead to severe damages on thymic epithelial cells (TECs), which result in delayed thymopoiesis and a prolonged period of T-cell immunodeficiency. Understanding the mechanisms that govern thymic regeneration is of paramount interest for the recovery of a functional immune system notably after bone marrow transplantation (BMT). Here, we show that RANK ligand (RANKL) is upregulated in CD4 thymocytes and lymphoid tissue inducer (LTi) cells during the early phase of thymic regeneration. Importantly, whereas RANKL neutralization alters TEC recovery after irradiation, RANKL administration during BMT boosts the regeneration of TEC subsets including thymic epithelial progenitor-enriched cells, thymus homing of lymphoid progenitors, and thymopoiesis. RANKL increases specifically in LTi cells, lymphotoxin α, which is critical for thymic regeneration. RANKL treatment, dependent on lymphotoxin α, is beneficial upon BMT in young and aged individuals. This study thus indicates that RANKL may be clinically useful to improve T-cell function recovery after BMT by controlling multiple facets of thymic regeneration.
[Mh] Termos MeSH primário: Transplante de Medula Óssea/efeitos adversos
Células Epiteliais/fisiologia
Ligante RANK/administração & dosagem
Radioterapia/efeitos adversos
Regeneração
Timo/fisiologia
[Mh] Termos MeSH secundário: Animais
Linfotoxina-alfa/metabolismo
Camundongos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphotoxin-alpha); 0 (RANK Ligand)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.15252/emmm.201607176


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[PMID]:29300739
[Au] Autor:Seeger H; Lindenmeyer MT; Cohen CD; Jaeckel C; Nelson PJ; Chen J; Edenhofer I; Kozakowski N; Regele H; Boehmig G; Brandt S; Wuethrich RP; Heikenwalder M; Fehr T; Segerer S
[Ad] Endereço:Division of Nephrology, University Hospital, Zuerich, Switzerland.
[Ti] Título:Lymphotoxin expression in human and murine renal allografts.
[So] Source:PLoS One;13(1):e0189396, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The kidney is the most frequently transplanted solid organ. Recruitment of inflammatory cells, ranging from diffuse to nodular accumulations with defined microarchitecture, is a hallmark of acute and chronic renal allograft injury. Lymphotoxins (LTs) mediate the communication of lymphocytes and stromal cells and play a pivotal role in chronic inflammation and formation of lymphoid tissue. The aim of this study was to assess the expression of members of the LT system in acute rejection (AR) and chronic renal allograft injury such as transplant glomerulopathy (TG) and interstitial fibrosis/tubular atrophy (IFTA). We investigated differentially regulated components in transcriptomes of human renal allograft biopsies. By microarray analysis, we found the upregulation of LTß, LIGHT, HVEM and TNF receptors 1 and 2 in AR and IFTA in human renal allograft biopsies. In addition, there was clear evidence for the activation of the NFκB pathway, most likely a consequence of LTß receptor stimulation. In human renal allograft biopsies with transplant glomerulopathy (TG) two distinct transcriptional patterns of LT activation were revealed. By quantitative RT-PCR robust upregulation of LTα, LTß and LIGHT was shown in biopsies with borderline lesions and AR. Immunohistochemistry revealed expression of LTß in tubular epithelial cells and inflammatory infiltrates in transplant biopsies with AR and IFTA. Finally, activation of LT signaling was reproduced in a murine model of renal transplantation with AR. In summary, our results indicate a potential role of the LT system in acute renal allograft rejection and chronic transplant injury. Activation of the LT system in allograft rejection in rodents indicates a species independent mechanism. The functional role of the LT system in acute renal allograft rejection and chronic injury remains to be determined.
[Mh] Termos MeSH primário: Transplante de Rim
Rim/metabolismo
Linfotoxina-alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Biópsia
DNA Complementar/genética
Rejeição de Enxerto
Seres Humanos
Glomérulos Renais/patologia
Transplante de Rim/efeitos adversos
Camundongos
Análise de Sequência com Séries de Oligonucleotídeos
RNA Mensageiro/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transplante Homólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Lymphotoxin-alpha); 0 (RNA, Messenger)
[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:180105
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189396


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[PMID]:28917655
[Au] Autor:Hu Z; Chen M; Zhou H; Tharakan A; Wang X; Qiu L; Liang S; Qin X; Zhang Y; Wang W; Xu Y; Ying Z
[Ad] Endereço:Department of Endocrinology, The People's Hospital of Zhengzhou University (Henan Provincial People's Hospital), Zhengzhou, Henan 450003, China; Department of Medicine Cardiology Division, University of Maryland School of Medicine, Baltimore, MD 21201, USA. Electronic address: huziying828@126.com.
[Ti] Título:Inactivation of TNF/LT locus alters mouse metabolic response to concentrated ambient PM .
[So] Source:Toxicology;390:100-108, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Exposure to ambient fine particulate matter (PM ) is associated with increased cardiometabolic morbidity and mortality. This is widely believed to be attributable to PM exposure-induced pulmonary and subsequent systemic inflammation. Tumor necrosis factor alpha (TNFα), lymphotoxin α (LTα), and lymphotoxin ß (LTß) are three homologous pro-inflammatory cytokines, each with both unique and redundant activities in inflammation. Their role in PM exposure-induced inflammation and adverse cardiometabolic effects has to be determined. METHODS AND RESULTS: LTα/TNFα/LTß triple-knockout (TNF/LT KO) and wildtype (WT) mice were exposed to concentrated ambient PM (CAP) for 5 months. Lung pathological analysis revealed that TNF/LT deficiency reduced CAP exposure-induced pulmonary inflammation. However, glucose homeostasis assessments showed that TNF/LT deficiency significantly aggravated CAP exposure-induced glucose intolerance and insulin resistance. Consistent with glucose homeostasis assessments, CAP exposure significantly increased the body weight and adiposity of TNF/LT KO but not WT mice. In contrast to its body weight effects, CAP exposure reduced food intake of WT but not TNF/LT KO mice. On the other hand, CAP exposure induced marked fat droplet accumulation in brown adipose tissues of WT mice and significantly decreased their uncoupling protein 1 (UCP1) expression, and these effects were markedly exacerbated in TNF/LT KO mice. CONCLUSION: The present study suggests that TNF/LT deficiency influences PM exposure-induced response of energy metabolism through alterations in both food intake and energy expenditure.
[Mh] Termos MeSH primário: Inativação Gênica
Transtornos do Metabolismo de Glucose/induzido quimicamente
Linfotoxina-alfa/deficiência
Linfotoxina-beta/deficiência
Obesidade/induzido quimicamente
Material Particulado/toxicidade
Pneumonia/prevenção & controle
Fator de Necrose Tumoral alfa/deficiência
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/efeitos dos fármacos
Tecido Adiposo Marrom/metabolismo
Tecido Adiposo Marrom/fisiopatologia
Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/metabolismo
Tecido Adiposo Branco/fisiopatologia
Adiposidade/efeitos dos fármacos
Animais
Biomarcadores/sangue
Glicemia/efeitos dos fármacos
Glicemia/metabolismo
Ingestão de Alimentos/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Genótipo
Transtornos do Metabolismo de Glucose/genética
Transtornos do Metabolismo de Glucose/metabolismo
Insulina/sangue
Resistência à Insulina
Gotículas Lipídicas/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Linfotoxina-alfa/genética
Linfotoxina-beta/genética
Camundongos Endogâmicos C57BL
Camundongos Knockout
Obesidade/genética
Obesidade/metabolismo
Obesidade/fisiopatologia
Tamanho da Partícula
Fenótipo
Pneumonia/induzido quimicamente
Pneumonia/genética
Pneumonia/metabolismo
Fatores de Tempo
Fator de Necrose Tumoral alfa/genética
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Insulin); 0 (Ltb protein, mouse); 0 (Lymphotoxin-alpha); 0 (Lymphotoxin-beta); 0 (Particulate Matter); 0 (Tumor Necrosis Factor-alpha); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE


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[PMID]:28640389
[Au] Autor:Wang FH; Wang Y; Sun GP; Chen JH; Lin YC; Liu W; Zheng RS; Chen J; Zhang HL; Lan HT; Qi J; Liu YQ; Deng YM; Zhao H; Xiong JP; Xu Q; Jiang WQ; Li YH
[Ad] Endereço:Department of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou, People's Republic of China.
[Ti] Título:Efficacy and safety of recombinant human lymphotoxin-α derivative with cisplatin and fluorouracil in patients with metastatic esophageal squamous cell carcinoma: A randomized, multicenter, open-label, controlled, phase 2b trial.
[So] Source:Cancer;123(20):3986-3994, 2017 Oct 15.
[Is] ISSN:1097-0142
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recombinant human lymphotoxin-α derivative (rhLTα-Da) is a lymphotoxin-α derivative that is missing 27 N-terminal amino acid residues. Previous studies indicated a benefit from the addition of rhLTα-Da to cisplatin-based treatment in patients with metastatic esophageal squamous cell carcinoma. The current study was conducted to evaluate the efficacy and safety of rhLTα-Da plus cisplatin and fluorouracil (PF) in patients with mESCC. METHODS: Patients from 15 centers in China were randomly assigned (1:1:1) to 3 arms (arm A, PF plus 10 µg/m daily rhLTα-Da; arm B, PF plus 20 µg/m daily rhLTα-Da; arm C, PF alone). The primary endpoints included progression-free survival (PFS) and the confirmed overall response rate (ORR). An exploratory analysis was performed to evaluate the role of serum tumor necrosis factor receptor II (TNFR II) in predicting the efficacy of rhLTα-Da. RESULTS: Between September 2010 and May 2013, 150 patients were enrolled. No significant differences in either PFS or ORR were observed between the 3 arms. However, in a small subset of patients who had low serum TNFR II levels, the median PFS was significantly longer for those in arm B than for these in other 2 arms (7.2 months [95% confidence interval, 5.1-8.6 months] for arm B vs 3.5 months [95% confidence interval, 1.7-5.5 months] for arm A [P = .022] and 4.0 months [95% confidence interval, 3.2-6.3 months] for arm C [P = .027]). The addition of rhLTα-Da significantly increased the incidence of chills (P < .001). CONCLUSIONS: rhLTα-Da combined with the PF regimen failed to improve PFS and ORR in patients with mESCC, except in a small subset that had low serum TNFR II concentrations. Cancer 2017;123:3986-94. © 2017 American Cancer Society.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma de Células Escamosas/tratamento farmacológico
Neoplasias Esofágicas/patologia
Linfotoxina-alfa/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/secundário
China
Cisplatino/administração & dosagem
Intervalo Livre de Doença
Neoplasias Esofágicas/metabolismo
Feminino
Fluoruracila/administração & dosagem
Seres Humanos
Linfotoxina-alfa/efeitos adversos
Masculino
Meia-Idade
Receptores Tipo II do Fator de Necrose Tumoral/sangue
Proteínas Recombinantes/efeitos adversos
Proteínas Recombinantes/uso terapêutico
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Lymphotoxin-alpha); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Recombinant Proteins); Q20Q21Q62J (Cisplatin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1002/cncr.30845


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[PMID]:28489756
[Au] Autor:Jia B; Qi X
[Ad] Endereço:aCenter of Hepatopathy, the First Hospital of Hebei Medical University bDepartment of Orthopaedics, The Third Hospital of Hebei Medical University, Shijiazhuang, China.
[Ti] Título:The genetic association between polymorphisms in lymphotoxin-α gene and ankylosing spondylitis susceptibility in Chinese group: A case-control study.
[So] Source:Medicine (Baltimore);96(19):e6796, 2017 May.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The study was designed to reveal the genetic relationship of lymphotoxin-α (LTA) polymorphisms with risk of ankylosing spondylitis (AS) in Chinese Han population.LTA polymorphisms were genotyped by polymerase chain reaction-direct sequencing (PCR-DS) in 138 AS patients and 141 healthy controls. The genotype distribution in control group was checked the status of Hardy-Weinberg equilibrium (HWE). Odds ratio (OR) with 95% confidence interval (95%CI) calculated by χ test was used to show effects of LTA polymorphisms on AS risk. Logistic regressive analysis was used to calculate the adjusted OR values. Additionally, the linkage disequilibrium of LTA polymorphisms was examined by Haploview.G allele of rs909253 was significantly higher frequency in AS patients (P = .02), which was associated with the increased risk of AS (OR = 1.53, 95%CI = 1.07-2.18). The carriages of GG genotype in rs909253 showed a high risk of AS occurrence, compared with AA genotype carriers (OR = 2.46, 95%CI = 1.13-5.35). Multivariate analysis demonstrated that the G allele (OR = 1.52, 95%CI = 1.05-2.15) and GG genotype (OR = 2.36, 95%CI = 1.06-5.24) of rs909253 were still positively associated with AS susceptibility. However, there was no significant association between AS risk and rs2239704 or rs2229094.LTA rs909253 polymorphism contributes to the occurrence of AS.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Linfotoxina-alfa/genética
Polimorfismo de Nucleotídeo Único
Espondilite Anquilosante/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
China
Feminino
Estudos de Associação Genética
Genótipo
Seres Humanos
Desequilíbrio de Ligação
Masculino
Meia-Idade
Espondilite Anquilosante/etnologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Lymphotoxin-alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006796


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[PMID]:28476436
[Au] Autor:Teos LY; Alevizos I
[Ad] Endereço:Sjögren's Syndrome and Salivary Gland Dysfunction Unit, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
[Ti] Título:Genetics of Sjögren's syndrome.
[So] Source:Clin Immunol;182:41-47, 2017 Sep.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pathogenesis of Sjögren's syndrome has not been elucidated. There has been evidence that genetics play an important role in the development of this disease from earlier studies. However, till now only a number of genes have been identified to be associated with SS, and these have only a weak or moderate effect. In this review we summarize the findings of the genetics studies and emphasize the need of large multicenter projects that will increase the sample sizes to provide more meaningful associations, as is the case in other common autoimmune diseases.
[Mh] Termos MeSH primário: Antígenos HLA/genética
Síndrome de Sjogren/genética
[Mh] Termos MeSH secundário: Fator Ativador de Células B/genética
Quimiocina CCL11/genética
Proteínas de Ligação a DNA/genética
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Fatores Reguladores de Interferon/genética
Subunidade p35 da Interleucina-12/genética
Linfotoxina-alfa/genética
Receptor 3 Desencadeador da Citotoxicidade Natural/genética
Ligante OX40/genética
Receptores CXCR5/genética
Fator de Transcrição STAT4/genética
Proteínas da Membrana Plasmática de Transporte de Serotonina/genética
Transativadores/genética
Fatores de Transcrição TFII/genética
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/genética
Quinases da Família src/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (CCL11 protein, human); 0 (CXCR5 protein, human); 0 (Chemokine CCL11); 0 (DNA-Binding Proteins); 0 (EBF1 protein, human); 0 (GTF2I protein, human); 0 (HLA Antigens); 0 (IL12A protein, human); 0 (IRF5 protein, human); 0 (Interferon Regulatory Factors); 0 (Interleukin-12 Subunit p35); 0 (Lymphotoxin-alpha); 0 (NCR3 protein, human); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (OX40 Ligand); 0 (Receptors, CXCR5); 0 (STAT4 Transcription Factor); 0 (STAT4 protein, human); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (TNFSF13B protein, human); 0 (TNFSF4 protein, human); 0 (TNIP1 protein, human); 0 (Trans-Activators); 0 (Transcription Factors, TFII); EC 2.7.10.2 (BLK protein, human); EC 2.7.10.2 (src-Family Kinases); EC 3.4.19.12 (TNFAIP3 protein, human); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


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[PMID]:28275260
[Au] Autor:Croft M; Siegel RM
[Ad] Endereço:Division of Immune Regulation, La Jolla Institute for Allergy and Immunology, and Department of Medicine, University of California San Diego, La Jolla, California 92037, USA.
[Ti] Título:Beyond TNF: TNF superfamily cytokines as targets for the treatment of rheumatic diseases.
[So] Source:Nat Rev Rheumatol;13(4):217-233, 2017 Apr.
[Is] ISSN:1759-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF blockers are highly efficacious at dampening inflammation and reducing symptoms in rheumatic diseases such as rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis, and also in nonrheumatic syndromes such as inflammatory bowel disease. As TNF belongs to a superfamily of 19 structurally related proteins that have both proinflammatory and anti-inflammatory activity, reagents that disrupt the interaction between proinflammatory TNF family cytokines and their receptors, or agonize the anti-inflammatory receptors, are being considered for the treatment of rheumatic diseases. Biologic agents that block B cell activating factor (BAFF) and receptor activator of nuclear factor-κB ligand (RANKL) have been approved for the treatment of systemic lupus erythematosus and osteoporosis, respectively. In this Review, we focus on additional members of the TNF superfamily that could be relevant for the pathogenesis of rheumatic disease, including those that can strongly promote activity of immune cells or increase activity of tissue cells, as well as those that promote death pathways and might limit inflammation. We examine preclinical mouse and human data linking these molecules to the control of damage in the joints, muscle, bone or other tissues, and discuss their potential as targets for future therapy of rheumatic diseases.
[Mh] Termos MeSH primário: Terapia de Alvo Molecular
Doenças Reumáticas/tratamento farmacológico
Doenças Reumáticas/imunologia
Fatores de Necrose Tumoral/antagonistas & inibidores
Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Ligante 4-1BB/antagonistas & inibidores
Ligante 4-1BB/metabolismo
Animais
Ligante CD27/antagonistas & inibidores
Ligante CD27/metabolismo
Ligante de CD40/antagonistas & inibidores
Ligante de CD40/metabolismo
Morte Celular
Citocina TWEAK
Células Dendríticas/imunologia
Proteína Ligante Fas/antagonistas & inibidores
Proteína Ligante Fas/metabolismo
Seres Humanos
Tolerância Imunológica
Ativação Linfocitária
Linfotoxina-alfa/antagonistas & inibidores
Linfotoxina-alfa/metabolismo
Ligante OX40/antagonistas & inibidores
Ligante OX40/metabolismo
Transdução de Sinais
Linfócitos T/imunologia
Ligante Indutor de Apoptose Relacionado a TNF/antagonistas & inibidores
Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/antagonistas & inibidores
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
Membro 15 da Superfamília de Ligantes de Fatores de Necrose Tumoral/antagonistas & inibidores
Membro 15 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (4-1BB Ligand); 0 (CD27 Ligand); 0 (Cytokine TWEAK); 0 (Fas Ligand Protein); 0 (Lymphotoxin-alpha); 0 (OX40 Ligand); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF12 protein, human); 0 (TNFSF18 protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (Tumor Necrosis Factor Ligand Superfamily Member 15); 0 (Tumor Necrosis Factors); 147205-72-9 (CD40 Ligand)
[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:170310
[St] Status:MEDLINE
[do] DOI:10.1038/nrrheum.2017.22


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[PMID]:28116918
[Au] Autor:Muratore F; Pipitone N; Salvarani C
[Ad] Endereço:a Rheumatology Unit, Department of Internal Medicine , Azienda Ospedaliera ASMN, Istituto di Ricovero e Cura a Carattere Scientifico , Reggio Emilia , Italy.
[Ti] Título:Standard and biological treatment in large vessel vasculitis: guidelines and current approaches.
[So] Source:Expert Rev Clin Immunol;13(4):345-360, 2017 Apr.
[Is] ISSN:1744-8409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Giant cell arteritis and Takayasu arteritis are the two major forms of idiopathic large vessel vasculitis. High doses of glucocorticoids are effective in inducing remission in both conditions, but relapses and recurrences are common, requiring prolonged glucocorticoid treatment with the risk of the related adverse events. Areas covered: In this article, we will review the standard and biological treatment strategies in large vessel vasculitis, and we will focus on the current approaches to these diseases. Expert commentary: The results of treatment trials with conventional immunosuppressive agents such as methotrexate, azathioprine, mycophenolate mofetil, and cyclophosphamide have overall been disappointing. TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis. Observational evidence strongly supports the use of anti-TNF-α agents and tocilizumab in Takayasu patients with relapsing disease. However biological agents are not curative, and relapses remain common.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Terapia Biológica/tendências
Arterite de Células Gigantes/terapia
Glucocorticoides/uso terapêutico
Imunossupressores/uso terapêutico
Arterite de Takayasu/terapia
[Mh] Termos MeSH secundário: Animais
Azatioprina/uso terapêutico
Ensaios Clínicos como Assunto
Seres Humanos
Linfotoxina-alfa/imunologia
Metotrexato/uso terapêutico
Guias de Prática Clínica como Assunto
Recidiva
Indução de Remissão
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Glucocorticoids); 0 (Immunosuppressive Agents); 0 (Lymphotoxin-alpha); MRK240IY2L (Azathioprine); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1080/1744666X.2017.1285699


  9 / 2872 MEDLINE  
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[PMID]:27941876
[Au] Autor:Yang J; Lu C; Wei J; Guo Y; Liu W; Luo L; Fisch G; Li X
[Ad] Endereço:Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York, NY, USA.
[Ti] Título:Inhibition of KPNA4 attenuates prostate cancer metastasis.
[So] Source:Oncogene;36(20):2868-2878, 2017 May 18.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Prostate cancer (PCa) is a common cancer in men. Although current treatments effectively palliate symptoms and prolong life, the metastatic PCa remains incurable. It is important to find biomarkers and targets to improve metastatic PCa diagnosis and treatment. Here we report a novel correlation between karyopherin α4 (KPNA4) and PCa pathological stages. KPNA4 mediates the cytoplasm-to-nucleus translocation of transcription factors, including nuclear factor kappa B, although its role in PCa was largely unknown. We find that knockdown of KPNA4 reduces cell migration in multiple PCa cell lines, suggesting a role of KPNA4 in PCa progression. Indeed, stable knockdown of KPNA4 significantly reduces PCa invasion and distant metastasis in mouse models. Functionally, KPNA4 alters tumor microenvironment in terms of macrophage polarization and osteoclastogenesis by modulating tumor necrosis factor (TNF)-α and -ß. Further, KPNA4 is proved as a direct target of miR-708, a tumor-suppressive microRNA. We disclose the role of miR-708-KPNA4-TNF axes in PCa metastasis and KPNA4's potential as a novel biomarker for PCa metastasis.
[Mh] Termos MeSH primário: Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
alfa Carioferinas/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular
Progressão da Doença
Expressão Gênica
Técnicas de Silenciamento de Genes
Inativação Gênica
Seres Humanos
Linfotoxina-alfa/metabolismo
Masculino
Camundongos
MicroRNAs/genética
Modelos Biológicos
Invasividade Neoplásica
Metástase Neoplásica
Neoplasias da Próstata/genética
Interferência de RNA
Fator de Necrose Tumoral alfa/metabolismo
alfa Carioferinas/genética
alfa Carioferinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KPNA4 protein, human); 0 (Lymphotoxin-alpha); 0 (MIRN708 microRNA, human); 0 (MicroRNAs); 0 (Tumor Necrosis Factor-alpha); 0 (alpha Karyopherins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171118
[Lr] Data última revisão:
171118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2016.440


  10 / 2872 MEDLINE  
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[PMID]:27913631
[Au] Autor:Wroblewska JA; Zhang Y; Tang H; Guo X; Nagler C; Fu YX
[Ad] Endereço:Committee on Immunology, University of Chicago, Chicago, IL 60637.
[Ti] Título:Cutting Edge: Lymphotoxin Signaling Is Essential for Clearance of Salmonella from the Gut Lumen and Generation of Anti-Salmonella Protective Immunity.
[So] Source:J Immunol;198(1):55-60, 2017 Jan 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The immunological components that control resolution of Salmonella infection and successful vaccination are poorly defined. In a model of chronic gastrointestinal infection, we observed that the lymphotoxin (LT) pathway is essential for the clearance and resolution of primary infection of attenuated Salmonella enterica Typhimurium strain SL3261 ΔaroA Using gnotobiotic mice, we show that LTß receptor (LTßR) signaling and the microbiota are required to promote clearance of attenuated S. enterica Typhimurium from the gut lumen. We also found that LTßR signaling was required for successful immunization and subsequent protection upon challenge with a virulent strain of S enterica Typhimurium. LTßR signaling promoted the development of specific IgG recognizing S enterica Typhimurium during infection, as well as Ag-driven IFN-γ responses. B cell- and type 3 innate lymphoid cell-derived LT signaling, but not T cell-derived LT, contributes to anti-S enterica Typhimurium protective responses. Collectively, our results suggest that LT signaling is essential for multiple steps of anti-S enterica Typhimurium immune responses.
[Mh] Termos MeSH primário: Microbioma Gastrointestinal/imunologia
Linfotoxina-alfa/imunologia
Salmonelose Animal/imunologia
[Mh] Termos MeSH secundário: Animais
Ensaio de Imunoadsorção Enzimática
Vida Livre de Germes
Camundongos
Salmonella typhimurium/imunologia
Transdução de Sinais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphotoxin-alpha)
[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:161204
[St] Status:MEDLINE



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