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[PMID]:29363152
[Au] Autor:Rodrigues Oliveira JL; Teixeira MM; Lambertucci JR; Antunes CMF; Carneiro M; Negrão-Corrêa D
[Ad] Endereço:Departamento de Parasitologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
[Ti] Título:Plasma levels of innate immune mediators are associated with liver fibrosis in low parasite burden Schistosoma mansoni-infected individuals.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the murine model, it was demonstrated that pro-inflammatory cytokines and chemokines are essential to the formation and modulation of Schistosoma-induced granulomatous inflammation. However, the relationship of these immune mediators and disease severity is hard to be established in naturally infected individuals. The current study evaluates the association between plasma concentrations of MIF, sTNF-R1, CCL3, CCL7 and CCL24 and schistosomiasis morbidity in Schistosoma mansoni-infected patients with a low parasite burden. For this propose, 97 S. mansoni-infected individuals were subjected to abdominal ultrasound analysis and clinical examination. Among them, 88 had plasma concentration of immune mediators estimated by ELISA assay. Multivariate linear regression models were used to evaluate the relationship between the plasma concentration of immune mediators and the variables investigated. Although most individuals presented low parasite burden, over 30% of them showed signs of fibrosis defined by ultrasound measurements and 2 patients had a severe form of schistosomiasis. No association between parasite burden and the plasma levels of chemokine/cytokines or disease severity was observed. There was a positive association between plasma concentration of CCL4, sTNF-R1, CCL3 and MIF with gall bladder thickness and/or with portal vein thickness that are liver fibrosis markers. In contrast, no association was found between CCL7 plasma concentrations with any of the schistosomiasis morbidity parameters evaluated. The data showed that CCL24, sTNFR1, MIF and CCL3 can be detected in plasma of S. mansoni-infected individuals and their concentration would be used as prognostic makers of Schistosoma-induced liver fibrosis, even in individuals with low parasite burden.
[Mh] Termos MeSH primário: Quimiocina CCL24/sangue
Quimiocina CCL3/sangue
Quimiocina CCL7/sangue
Oxirredutases Intramoleculares/sangue
Cirrose Hepática/imunologia
Fatores Inibidores da Migração de Macrófagos/sangue
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
Schistosoma mansoni/imunologia
Esquistossomose mansoni/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Animais
Seres Humanos
Fígado/irrigação sanguínea
Fígado/parasitologia
Fígado/patologia
Cirrose Hepática/parasitologia
Meia-Idade
Veia Porta/patologia
Esquistossomose mansoni/parasitologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL24 protein, human); 0 (CCL3 protein, human); 0 (CCL7 protein, human); 0 (Chemokine CCL24); 0 (Chemokine CCL3); 0 (Chemokine CCL7); 0 (Macrophage Migration-Inhibitory Factors); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (TNFRSF1A protein, human); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (MIF protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12642


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[PMID]:28454496
[Au] Autor:La Torre F; Caparello MC; Cimaz R
[Ad] Endereço:a Pediatric Rheumatology Regional Center, Department of Pediatrics , Antonio Perrino Hospital , Brindisi , Puglia , Italy.
[Ti] Título:Canakinumab for the treatment of TNF-receptor associated periodic syndrome.
[So] Source:Expert Rev Clin Immunol;13(6):513-523, 2017 06.
[Is] ISSN:1744-8409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: TNF-receptor-associated periodic syndrome is an autoinflammatory disorder caused by mutations in TNF receptor superfamily 1A gene. The molecular pathogenesis of TRAPS remains unclear; it is known that a key role is played by mutations in TNFRSF1A that induce the hypersecretion of pro-inflammatory cytokines as well as IL-1ß, resulting in uncontrolled inflammatory reactions. Furthermore, TNFRSF1A gene mutations result in intracellular stress ultimately leading to increased production of interleukin-1ß, but the exact mechanism referred to in the connection between TNFRSF1A mutation and increased release of IL-1ß, is still under study. This explains why IL-1 inhibition treatment can be effective in treating TRAPS patients. The purpose of this review is to discuss the safety and efficacy of canakinumab, a high-affinity human monoclonal anti IL-1ß antibody. Areas covered: The data obtained from case reports, case series, Phase II study and a phase III randomized, double-blind, placebo controlled trial have been analyzed. Efficacy and safety profiles of canakinumab are discussed. Expert commentary: Was discussed an overview of treatment options in TRAPS patients. The understanding of pathogenesis of TNF-receptor-associated periodic syndrome led to realize why TRAPS patients respond to IL-1 inhibition. Canakinumab became approved for the treatment in TRAPS patients very recently.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Anticorpos Monoclonais/uso terapêutico
Febre/terapia
Doenças Hereditárias Autoinflamatórias/terapia
Imunoterapia/métodos
Interleucina-1beta/imunologia
[Mh] Termos MeSH secundário: Ensaios Clínicos como Assunto
Aprovação de Drogas
Febre/genética
Febre/imunologia
Doenças Hereditárias Autoinflamatórias/genética
Doenças Hereditárias Autoinflamatórias/imunologia
Seres Humanos
Mutação/genética
Receptores Tipo I de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antibodies, Monoclonal); 0 (Interleukin-1beta); 0 (Receptors, Tumor Necrosis Factor, Type I); 37CQ2C7X93 (canakinumab)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1080/1744666X.2017.1324783


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[PMID]:28747340
[Au] Autor:Bradford EM; Ryu SH; Singh AP; Lee G; Goretsky T; Sinh P; Williams DB; Cloud AL; Gounaris E; Patel V; Lamping OF; Lynch EB; Moyer MP; De Plaen IG; Shealy DJ; Yang GY; Barrett TA
[Ad] Endereço:Department of Internal Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL 60611.
[Ti] Título:Epithelial TNF Receptor Signaling Promotes Mucosal Repair in Inflammatory Bowel Disease.
[So] Source:J Immunol;199(5):1886-1897, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF plays an integral role in inflammatory bowel disease (IBD), as evidenced by the dramatic therapeutic responses in Crohn's disease (CD) patients induced by chimeric anti-TNF mAbs. However, treatment of CD patients with etanercept, a decoy receptor that binds soluble TNF, fails to improve disease. To explore this discrepancy, we investigated the role of TNF signaling in Wnt/ß-catenin-mediated intestinal stem cell and progenitor cell expansion in CD patients, human cells, and preclinical mouse models. We hypothesized that TNF exerts beneficial effects on intestinal epithelial cell (IEC) responses to injury. In CD patients, intestinal stem cell and progenitor cell Wnt/ß-catenin signaling correlates with inflammation status. TNF-deficient ( ) mice exhibited increased apoptosis, less IEC proliferation, and less Wnt signaling when stimulated with anti-CD3 mAb. Bone marrow (BM) chimera mice revealed that mucosal repair depended on TNF production by BM-derived cells and TNFR expression by radioresistant IECs. Wild-type→ BM chimera mice with chronic dextran sodium sulfate colitis exhibited delayed ulcer healing, more mucosal inflammation, and impaired Wnt/ß-catenin signaling, consistent with the hypothesis that epithelial TNFR signaling participates in mucosal healing. The direct effect of TNF on stem cells was demonstrated by studies of TNF-induced Wnt/ß-catenin target gene expression in murine enteroids and colonoid cultures and TNF-induced ß-catenin activation in nontransformed human NCM460 cells (TOPFlash) and mice (TOP-GAL). Together, these data support the hypothesis that TNF plays a beneficial role in enhancing Wnt/ß-catenin signaling during ulcer healing in IBD. These novel findings will inform clinicians and therapeutic chemists alike as they strive to develop novel therapies for IBD patients.
[Mh] Termos MeSH primário: Células-Tronco Adultas/fisiologia
Anticorpos Monoclonais/uso terapêutico
Colite/imunologia
Células Epiteliais/fisiologia
Doenças Inflamatórias Intestinais/imunologia
Mucosa Intestinal/fisiologia
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/metabolismo
Linhagem Celular
Sulfato de Dextrana
Seres Humanos
Doenças Inflamatórias Intestinais/terapia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo II do Fator de Necrose Tumoral/genética
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Proteínas Wnt/metabolismo
Cicatrização
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); 0 (Tumor Necrosis Factor-alpha); 0 (Wnt Proteins); 0 (beta Catenin); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601066


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[PMID]:28453789
[Au] Autor:Dhamoon MS; Cheung YK; Moon YP; Wright CB; Willey JZ; Sacco RL; Elkind MSV
[Ti] Título:Association Between Serum Tumor Necrosis Factor Receptor 1 and Trajectories of Functional Status: The Northern Manhattan Study.
[So] Source:Am J Epidemiol;186(1):11-20, 2017 Jul 01.
[Is] ISSN:1476-6256
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We hypothesized that tumor necrosis factor receptor 1 (TNFR1) levels are associated with long-term trajectories of functional status independently of vascular risk factors and the occurrence of stroke and myocardial infarction (MI) during follow-up. In the Northern Manhattan Study, stroke-free persons aged ≥40 years in northern Manhattan (New York, New York) had annual assessments with the Barthel index (BI) for a median of 13 years (1993-2015). Assessment of baseline demographic factors, risk factors, and laboratory studies included measurement of TNFR1 (n = 1,863). Generalized estimating equations models were used to estimate standardized associations between TNFR1 and 1) baseline functional status and 2) change in function over time, adjusting for demographic factors, vascular risk factors, social variables, cognition, and depression, as well as stroke and MI occurrence during follow-up. The mean age of participants was 70 (standard deviation (SD), 10) years; 66% were women, and 55% were Hispanic. The mean TNFR1 level was 2.57 mg/L. TNFR1 was associated with baseline BI (-0.93 BI points per SD increment in TNFR1; 95% confidence interval: -1.59, -0.26) and change over time (-0.36 BI points per year per SD increment in TNFR1; 95% confidence interval: -0.69, -0.03). In this large population-based study, higher TNFR1 levels were associated with greater baseline disability and disability over time, even with adjustment for baseline covariates and stroke and MI occurrence during follow-up.
[Mh] Termos MeSH primário: Pessoas com Deficiência/estatística & dados numéricos
Nível de Saúde
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
[Mh] Termos MeSH secundário: Atividades Cotidianas
Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Índice de Massa Corporal
Cognição
Comorbidade
Depressão/epidemiologia
Feminino
Comportamentos Relacionados com a Saúde
Seres Humanos
Relações Interpessoais
Masculino
Meia-Idade
Infarto do Miocárdio/epidemiologia
Cidade de Nova Iorque/epidemiologia
Estudos Prospectivos
Fatores de Risco
Fatores Sexuais
Fatores Socioeconômicos
Acidente Vascular Cerebral/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor, Type I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/aje/kwx035


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[PMID]:29040328
[Au] Autor:Peuhu E; Salomaa SI; De Franceschi N; Potter CS; Sundberg JP; Pouwels J
[Ad] Endereço:Turku Centre for Biotechnology, University of Turku, Turku, Finland.
[Ti] Título:Integrin beta 1 inhibition alleviates the chronic hyperproliferative dermatitis phenotype of SHARPIN-deficient mice.
[So] Source:PLoS One;12(10):e0186628, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SHARPIN (Shank-Associated RH Domain-Interacting Protein) is a component of the linear ubiquitin chain assembly complex (LUBAC), which enhances TNF-induced NF-κB activity. SHARPIN-deficient (Sharpincpdm/cpdm) mice display multi-organ inflammation and chronic proliferative dermatitis (cpdm) due to TNF-induced keratinocyte apoptosis. In cells, SHARPIN also inhibits integrins independently of LUBAC, but it has remained enigmatic whether elevated integrin activity levels in the dermis of Sharpincpdm/cpdm mice is due to increased integrin activity or is secondary to inflammation. In addition, the functional contribution of increased integrin activation to the Sharpincpdm/cpdm phenotype has not been investigated. Here, we find increased integrin activity in keratinocytes from Tnfr1-/- Sharpincpdm/cpdm double knockout mice, which do not display chronic inflammation or proliferative dermatitis, thus suggesting that SHARPIN indeed acts as an integrin inhibitor in vivo. In addition, we present evidence for a functional contribution of integrin activity to the Sharpincpdm/cpdm skin phenotype. Treatment with an integrin beta 1 function blocking antibody reduced epidermal hyperproliferation and epidermal thickness in Sharpincpdm/cpdm mice. Our data indicate that, while TNF-induced cell death triggers the chronic inflammation and proliferative dermatitis, absence of SHARPIN-dependent integrin inhibition exacerbates the epidermal hyperproliferation in Sharpincpdm/cpdm mice.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
Dermatite/tratamento farmacológico
Epiderme/efeitos dos fármacos
Integrina beta1/genética
Queratinócitos/efeitos dos fármacos
Receptores Tipo I de Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/farmacologia
Apoptose
Proteínas de Transporte/imunologia
Proliferação Celular
Doença Crônica
Dermatite/genética
Dermatite/imunologia
Dermatite/patologia
Epiderme/imunologia
Epiderme/patologia
Feminino
Deleção de Genes
Regulação da Expressão Gênica
Inflamação
Integrina beta1/imunologia
Queratinócitos/imunologia
Queratinócitos/patologia
Masculino
Camundongos
Camundongos Knockout
NF-kappa B/genética
NF-kappa B/imunologia
Fenótipo
Receptores Tipo I de Fatores de Necrose Tumoral/deficiência
Receptores Tipo I de Fatores de Necrose Tumoral/imunologia
Transdução de Sinais
Ubiquitina/genética
Ubiquitina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Carrier Proteins); 0 (Integrin beta1); 0 (NF-kappa B); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Sipl1 protein, mouse); 0 (Tnfrsf1a protein, mouse); 0 (Ubiquitin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186628


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[PMID]:28964327
[Au] Autor:Nevalainen J; Korpimaki T; Kouru H; Sairanen M; Ryynanen M
[Ad] Endereço:Department of Obstetrics and Gynecology, Oulu University Hospital, Finland. Electronic address: marttjaa@paju.oulu.fi.
[Ti] Título:Performance of first trimester biochemical markers and mean arterial pressure in prediction of early-onset pre-eclampsia.
[So] Source:Metabolism;75:6-15, 2017 Oct.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To develop a predictive risk model for early-onset pre-eclampsia (EO-PE) using maternal characteristics, combined screening markers, previously reported biomarkers for PE and mean arterial pressure (MAP). METHODS: This retrospective study was conducted at Oulu University hospital between 2006 and 2010. Maternal serum from first trimester combined screening was further analyzed for alpha fetoprotein (AFP), placental growth factor (PlGF), soluble tumor necrosis factor receptor-1 (sTNFR1), retinol binding protein-4 (RBP4), a disintegrin and metalloprotease-12 (ADAM12), soluble P-selectin (sP-selectin), follistatin like-3 (FSTL3), adiponectin, angiopoietin-2 (Ang-2) and sex hormone binding globulin (SHBG). First, the training sample set with 29 cases of EO-PE and 652 controls was developed to study whether these biomarkers separately or in combination with prior risk (maternal characteristics, first trimester pregnancy associated plasma protein-A (PAPP-A) and free beta human chorionic gonadotrophin (fß-hCG)) could be used to predict the development of EO-PE. Second, the developed risk models were validated with a test sample set of 42 EO-PE and 141 control subjects. For the test set MAP data was also available. RESULTS: Single marker statistically significant (ANOVA p<0.05) changes between control and EO-PE pregnancies were observed with AFP, RBP4 and sTNFR1 with both training and test sample sets. Based on the test sample set performances, the best detection rate, 47% for a 10% false positive rate, was achieved with PlGF and sTNFR1 added with prior risk and MAP. CONCLUSION: Based on our results, the best first trimester biomarkers to predict the subsequent EO-PE were AFP, PlGF, RBP4 and sTNFR1. The risk models that performed best for the prediction of EO-PE included prior risk, MAP, sTNFR1 and AFP or PlGF or RBP4.
[Mh] Termos MeSH primário: Pressão Arterial/fisiologia
Pré-Eclâmpsia/diagnóstico
Valor Preditivo dos Testes
Primeiro Trimestre da Gravidez/sangue
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Estudos de Casos e Controles
Diagnóstico Precoce
Feminino
Seres Humanos
Proteínas de Membrana/sangue
Pré-Eclâmpsia/sangue
Gravidez
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
Proteínas Plasmáticas de Ligação ao Retinol/análise
Estudos Retrospectivos
alfa-Fetoproteínas/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AFP protein, human); 0 (Biomarkers); 0 (Membrane Proteins); 0 (PIGF protein, human); 0 (RBP4 protein, human); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Retinol-Binding Proteins, Plasma); 0 (alpha-Fetoproteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


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[PMID]:28920954
[Au] Autor:Menon MB; Gropengießer J; Fischer J; Novikova L; Deuretzbacher A; Lafera J; Schimmeck H; Czymmeck N; Ronkina N; Kotlyarov A; Aepfelbacher M; Gaestel M; Ruckdeschel K
[Ad] Endereço:Institute of Cell Biochemistry, Hannover Medical School, Hannover 30625, Germany.
[Ti] Título:p38 /MK2-dependent phosphorylation controls cytotoxic RIPK1 signalling in inflammation and infection.
[So] Source:Nat Cell Biol;19(10):1248-1259, 2017 Oct.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Receptor-interacting protein kinase-1 (RIPK1), a master regulator of cell fate decisions, was identified as a direct substrate of MAPKAP kinase-2 (MK2) by phosphoproteomic screens using LPS-treated macrophages and stress-stimulated embryonic fibroblasts. p38 /MK2 interact with RIPK1 in a cytoplasmic complex and MK2 phosphorylates mouse RIPK1 at Ser321/336 in response to pro-inflammatory stimuli, such as TNF and LPS, and infection with the pathogen Yersinia enterocolitica. MK2 phosphorylation inhibits RIPK1 autophosphorylation, curtails RIPK1 integration into cytoplasmic cytotoxic complexes, and suppresses RIPK1-dependent apoptosis and necroptosis. In Yersinia-infected macrophages, RIPK1 phosphorylation by MK2 protects against infection-induced apoptosis, a process targeted by Yersinia outer protein P (YopP). YopP suppresses p38 /MK2 activation to increase Yersinia-driven apoptosis. Hence, MK2 phosphorylation of RIPK1 is a crucial checkpoint for cell fate in inflammation and infection that determines the outcome of bacteria-host cell interaction.
[Mh] Termos MeSH primário: Apoptose
Inflamação/enzimologia
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Macrófagos/enzimologia
Proteínas Serina-Treonina Quinases/metabolismo
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Yersiniose/enzimologia
Yersinia enterocolitica/patogenicidade
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteínas de Bactérias/metabolismo
Citosol/enzimologia
Citosol/microbiologia
Feminino
Genótipo
Células HEK293
Interações Hospedeiro-Patógeno
Seres Humanos
Quinase I-kappa B/metabolismo
Inflamação/patologia
Peptídeos e Proteínas de Sinalização Intracelular/deficiência
Peptídeos e Proteínas de Sinalização Intracelular/genética
MAP Quinase Quinase Quinases/metabolismo
Macrófagos/efeitos dos fármacos
Macrófagos/microbiologia
Macrófagos/patologia
Masculino
Proteínas de Membrana/metabolismo
Camundongos Knockout
Necrose
Fenótipo
Fosforilação
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Serina-Treonina Quinases/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Serina
Transdução de Sinais
Fatores de Tempo
Transfecção
Fator de Necrose Tumoral alfa/toxicidade
Yersiniose/microbiologia
Yersiniose/patologia
Yersinia enterocolitica/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Tnfrsf1a protein, mouse); 0 (Tumor Necrosis Factor-alpha); 0 (Yop proteins translocation protein P, Yersinia); 452VLY9402 (Serine); EC 2.7.1.- (MAP-kinase-activated kinase 2); EC 2.7.1.- (MAP-kinase-activated kinase 3); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 2.7.11.1 (Ripk1 protein, mouse); EC 2.7.11.10 (I-kappa B Kinase); EC 2.7.11.10 (Ikbkb protein, mouse); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3614


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[PMID]:28920952
[Au] Autor:Dondelinger Y; Delanghe T; Rojas-Rivera D; Priem D; Delvaeye T; Bruggeman I; Van Herreweghe F; Vandenabeele P; Bertrand MJM
[Ad] Endereço:Inflammation Research Center, VIB, Technologiepark 927, Zwijnaarde-Ghent 9052, Belgium.
[Ti] Título:MK2 phosphorylation of RIPK1 regulates TNF-mediated cell death.
[So] Source:Nat Cell Biol;19(10):1237-1247, 2017 Oct.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders can, in certain conditions, be attributed to RIPK1 kinase-dependent cell death. Survival, however, is the default response of most cells to TNF stimulation, indicating that cell demise is normally actively repressed and that specific checkpoints must be turned off for cell death to proceed. We identified RIPK1 as a direct substrate of MK2 in the TNFR1 signalling pathway. Phosphorylation of RIPK1 by MK2 limits cytosolic activation of RIPK1 and the subsequent assembly of the death complex that drives RIPK1 kinase-dependent apoptosis and necroptosis. In line with these in vitro findings, MK2 inactivation greatly sensitizes mice to the cytotoxic effects of TNF in an acute model of sterile shock caused by RIPK1-dependent cell death. In conclusion, we identified MK2-mediated RIPK1 phosphorylation as an important molecular mechanism limiting the sensitivity of the cells to the cytotoxic effects of TNF.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Choque/induzido quimicamente
Fator de Necrose Tumoral alfa/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Citosol/enzimologia
Modelos Animais de Doenças
Ativação Enzimática
Feminino
Fibroblastos/enzimologia
Fibroblastos/patologia
Peptídeos e Proteínas de Sinalização Intracelular/antagonistas & inibidores
Peptídeos e Proteínas de Sinalização Intracelular/genética
Camundongos
Camundongos Endogâmicos C57BL
Necrose
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Proteínas Serina-Treonina Quinases/genética
Proteína Serina-Treonina Quinases de Interação com Receptores/antagonistas & inibidores
Proteína Serina-Treonina Quinases de Interação com Receptores/genética
Receptores Tipo I de Fatores de Necrose Tumoral/agonistas
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Serina
Choque/enzimologia
Choque/patologia
Choque/prevenção & controle
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intracellular Signaling Peptides and Proteins); 0 (Protein Kinase Inhibitors); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Tnfrsf1a protein, mouse); 0 (Tumor Necrosis Factor-alpha); 452VLY9402 (Serine); EC 2.7.1.- (MAP-kinase-activated kinase 2); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 2.7.11.1 (Ripk1 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3608


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[PMID]:28898696
[Au] Autor:Boege Y; Malehmir M; Healy ME; Bettermann K; Lorentzen A; Vucur M; Ahuja AK; Böhm F; Mertens JC; Shimizu Y; Frick L; Remouchamps C; Mutreja K; Kähne T; Sundaravinayagam D; Wolf MJ; Rehrauer H; Koppe C; Speicher T; Padrissa-Altés S; Maire R; Schattenberg JM; Jeong JS; Liu L; Zwirner S; Boger R; Hüser N; Davis RJ; Müllhaupt B; Moch H; Schulze-Bergkamen H; Clavien PA; Werner S; Borsig L; Luther SA; Jost PJ; Weinlich R; Unger K; Behrens A; Hillert L; Dillon C; Di Virgilio M; Wallach D; Dejardin E; Zender L; Naumann M; Walczak H; Green DR; Lopes M; Lavrik I
[Ad] Endereço:Department of Pathology and Molecular Pathology, University and University Hospital Zurich, 8091 Zurich, Switzerland.
[Ti] Título:A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development.
[So] Source:Cancer Cell;32(3):342-359.e10, 2017 Sep 11.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apoptotic function of caspase-8, but no caspase-3 or caspase-8 cleavage. It may represent a DNA damage-sensing mechanism in hepatocytes that can act via JNK and subsequent phosphorylation of the histone variant H2AX.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Carcinogênese/patologia
Caspase 8/metabolismo
Dano ao DNA
Neoplasias Hepáticas/enzimologia
Neoplasias Hepáticas/patologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Carcinoma Hepatocelular/patologia
Proliferação Celular
Senescência Celular
Doença Crônica
Cruzamentos Genéticos
Reparo do DNA
Proteína de Domínio de Morte Associada a Fas/metabolismo
Feminino
Instabilidade Genômica
Hepatectomia
Hepatócitos/patologia
Histonas/metabolismo
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Fígado/metabolismo
Fígado/patologia
Regeneração Hepática
Masculino
Camundongos
Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo
Fosforilação
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fadd protein, mouse); 0 (Fas-Associated Death Domain Protein); 0 (Histones); 0 (Mcl1 protein, mouse); 0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (gamma-H2AX protein, mouse); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases); EC 2.7.11.1 (Ripk1 protein, mouse); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.4.22.- (Caspase 8)
[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:170913
[St] Status:MEDLINE


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[PMID]:28886201
[Au] Autor:Quinn KM; Kan WT; Watson KA; Liddicoat BJ; Swan NG; McQuilten H; Denton AE; Li J; Chen W; Brown LE; Jackson DC; Reading PC; Doherty PC; Kedzierska K; Kedzierski L; Turner SJ; La Gruta NL
[Ad] Endereço:Infection and Immunity Program and Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
[Ti] Título:Extrinsically derived TNF is primarily responsible for limiting antiviral CD8+ T cell response magnitude.
[So] Source:PLoS One;12(9):e0184732, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TNF is a pro-inflammatory cytokine produced by both lymphoid and non-lymphoid cells. As a consequence of the widespread expression of its receptors (TNFR1 and 2), TNF plays a role in many important biological processes. In the context of influenza A virus (IAV) infection, TNF has variably been implicated in mediating immunopathology as well as suppression of the immune response. Although a number of cell types are able to produce TNF, the ability of CD8+ T cells to produce TNF following viral infection is a hallmark of their effector function. As such, the regulation and role of CD8+ T cell-derived TNF following viral infection is of great interest. Here, we show that the biphasic production of TNF by CD8+ T cells following in vitro stimulation corresponds to distinct patterns of epigenetic modifications. Further, we show that a global loss of TNF during IAV infection results in an augmentation of the peripheral virus-specific CD8+ T cell response. Subsequent adoptive transfer experiments demonstrated that this attenuation of the CD8+ T cell response was largely, but not exclusively, conferred by extrinsic TNF, with intrinsically-derived TNF making only modest contributions. In conclusion, TNF exerts an immunoregulatory role on CD8+ T cell responses following IAV infection, an effect that is largely mediated by extrinsically-derived TNF.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Imunoprecipitação da Cromatina
Feminino
Vírus da Influenza A/patogenicidade
Camundongos
Camundongos Endogâmicos C57BL
RNA Polimerase II/metabolismo
Receptores Tipo I de Fatores de Necrose Tumoral/metabolismo
Receptores Tipo II do Fator de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (Receptors, Tumor Necrosis Factor, Type II); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184732



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