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[PMID]:29441964
[Au] Autor:Kono Y; Miyoshi S; Fujita T
[Ti] Título:Dextran sodium sulfate alters cytokine production in macrophages .
[So] Source:Pharmazie;71(11):619-624, 2016 Nov 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Macrophages have been assumed to have a crucial role in the development of inflammatory bowel disease (IBD). However, involvement of intestinal macrophages in IBD onset and functional alterations of macrophages during IBD development has not been clarified. We investigated the effect of exposure of compounds used in the induction of colitis in mice on the immune responses of peritoneal macrophages in mice. 2,4,6- trinitrobenzenesulfonic acid and oxazolone did not affect the production of interleukin (IL)-10 and IL-12 from lipopolysaccharide (LPS)-stimulated peritoneal macrophages from BALB/c mice. A significant increase in IL-10 secretion and decrease in IL-12 production from LPS-stimulated macrophages were observed upon exposure to dextran sodium sulfate (DSS). TNF-α production was enhanced significantly by exposure to DSS and LPS. The level of nitric-oxide production from macrophages was increased slightly by exposure to DSS and LPS. Expression of sphingosine kinase-1 and LIGHT (both of which are specific biomarkers of M2b macrophages) was observed in macrophages upon DSS exposure. Alteration of cytokine production in macrophages was observed upon DSS exposure in the absence of LPS stimulation. Peritoneal macrophages from C57BL/6 mice showed similar responses to peritoneal macrophages from BALB/c mice against DSS. These results suggest that DSS directs the immune response of macrophages towards the M2b phenotype.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Sulfato de Dextrana/farmacologia
Macrófagos Peritoneais/metabolismo
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Colite/patologia
Feminino
Técnicas In Vitro
Interleucina-10/biossíntese
Interleucina-10/genética
Interleucina-12/biossíntese
Interleucina-12/genética
Lipopolissacarídeos/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Óxido Nítrico/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/biossíntese
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Especificidade da Espécie
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/biossíntese
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 31C4KY9ESH (Nitric Oxide); 9042-14-2 (Dextran Sulfate); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6688


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[PMID]:28422285
[Au] Autor:Chen W; Lv X; Liu C; Chen R; Liu J; Dai H; Zou GM
[Ad] Endereço:Xinhua Hospital, Shanghai Institute of Pediatric Research, Shanghai, China.
[Ti] Título:Hematopoietic stem/progenitor cell differentiation towards myeloid lineage is modulated by LIGHT/LIGHT receptor signaling.
[So] Source:J Cell Physiol;233(2):1095-1103, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytokine LT-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells (LIGHT) is a member of the tumor necrosis factor (TNF) superfamily. It is expressed primarily on activated T lymphocytes, and detectable on monocytes, granulocytes, and immune dendritic cells. It mainly plays a role in immune regulation including T cell activation and dendritic cell maturation. We recently reported its role as an inducer in embryonic stem cell differentiation, but its role in regulation of adult stem cell has not been defined. In the present study, we examined the expression of LIGHT receptor in Lin c-kit Sca-1 hematopoietic stem/progenitor cells (HSC/HPCs). We found that HSC express HVEM, a LIGHT receptor, on its surface. We further identified the role of LIGHT in promoting myeloid differentiation of HSCs driven by granulocyte-monocyte colony stimulating factor (GM-CSF). Further studies showed that LIGHT enhances both GM-CSF and GM-CSF receptor (GM-CSFR) expression in HSCs. LIGHT stimulation increases PU.1 expression in HSC/HPCs. In vivo administration of LIGHT increases the colony-forming unit-granulocyte/monocyte (CFU-GM) colony formation and plasma GM-CSF level. Altogether, the data suggest LIGHT promote myeloid differentiation of HSC/HPCs.
[Mh] Termos MeSH primário: Diferenciação Celular
Linhagem da Célula
Células-Tronco Hematopoéticas/metabolismo
Células Mieloides/metabolismo
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
Transdução de Sinais
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/metabolismo
Proliferação Celular
Células Cultivadas
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Masculino
Proteínas de Membrana/metabolismo
Camundongos Endogâmicos C57BL
Fenótipo
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/metabolismo
Transativadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Ly6a protein, mouse); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Tnfrsf14 protein, mouse); 0 (Tnfsf14 protein, mouse); 0 (Trans-Activators); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (proto-oncogene protein Spi-1); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25967


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[PMID]:28892469
[Au] Autor:Johansson-Percival A; He B; Li ZJ; Kjellén A; Russell K; Li J; Larma I; Ganss R
[Ad] Endereço:Harry Perkins Institute of Medical Research, Centre for Medical Research, The University of Western Australia, Nedlands, Western Australia, Australia.
[Ti] Título:De novo induction of intratumoral lymphoid structures and vessel normalization enhances immunotherapy in resistant tumors.
[So] Source:Nat Immunol;18(11):1207-1217, 2017 Nov.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor microenvironment confers profound resistance to anti-cancer immunotherapy. By targeting LIGHT, a member of the TNF superfamily of cytokines, to tumor vessels via a vascular targeting peptide (VTP), we developed a reagent with the dual ability to modulate the angiogenic vasculature and to induce tertiary lymphoid structures (TLSs). LIGHT-VTP triggered the influx of endogenous T cells into autochthonous or syngeneic tumors, which are resistant to immunotherapy. LIGHT-VTP in combination with checkpoint inhibition generated a large number of intratumoral effector and memory T cells with ensuing survival benefits, while the addition of anti-tumor vaccination achieved maximal therapeutic efficacy. Thus, the combination treatments stimulated the trafficking of pre-existing endogenous effector T cells as well as their intratumoral activation and were more successful than current immunotherapies, which fail due to tumor-intrinsic resistance mechanisms.
[Mh] Termos MeSH primário: Imunoterapia/métodos
Linfócitos/imunologia
Neoplasias/terapia
Neovascularização Patológica/terapia
Microambiente Tumoral/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Vacinas Anticâncer/administração & dosagem
Vacinas Anticâncer/farmacologia
Resistência a Medicamentos Antineoplásicos/imunologia
Quimioterapia Combinada
Linfócitos/metabolismo
Camundongos Endogâmicos C3H
Camundongos Transgênicos
Neoplasias/irrigação sanguínea
Neoplasias/imunologia
Neovascularização Patológica/imunologia
Peptídeos/administração & dosagem
Peptídeos/genética
Peptídeos/farmacologia
Análise de Sobrevida
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Linfócitos T/metabolismo
Resultado do Tratamento
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/química
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cancer Vaccines); 0 (Peptides); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14)
[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:170912
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3836


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[PMID]:28642135
[Au] Autor:Yuan X; Gu Y; Lai X; Gu Q
[Ad] Endereço:Heart Failure Center, Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital, Chengdu, 610072, China.
[Ti] Título:LIGHT is increased in patients with coronary disease and regulates inflammatory response and lipid metabolism in oxLDL-induced THP-1 macrophages.
[So] Source:Biochem Biophys Res Commun;490(3):732-738, 2017 Aug 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation is critical for the progression of hyperlipidemia. Although the exact mechanism through which inflammation affects hyperlipidemia is not very clear, evidence suggests that the tumor necrosis factor superfamily member 14 (TNFSF14/LIGHT)LIGHT might regulate lipid metabolism. In this study we investigated the expression of LIGHT in patients with different stages of coronary disease. The expression of lipid metabolism-related enzymes and inflammation-related proteins were further explored in oxidized low-density lipoproteins (oxLDL)-induced THP-1 macrophages. We found that LIGHT is highly expressed and companied with severe inflammations in patients with coronary disease. LIGHT significantly enhanced inflammation response in oxLDL-induced THP-1 macrophages. We further demonstrated that LIGHT markedly decreased the levels of lipolytic genes and increased the expressions of lipogenic genes in oxLDL-induced THP-1 macrophages. In addition, our results showed that LIGHT exerts its pro-inflammatory and pro-lipogenesis roles through activating nuclear factor-kappa B (NF-κB) signaling pathway. Taken together our study has demonstrated that LIGHT NF-κB-dependently exacerbates inflammation response and promotes lipid accumulation, and provided a new potential target for treatment of hyperlipidemia-related disease.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/imunologia
Hiperlipidemias/imunologia
Inflamação/imunologia
Lipoproteínas LDL/imunologia
Macrófagos/imunologia
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular
Doença da Artéria Coronariana/complicações
Seres Humanos
Hiperlipidemias/complicações
Inflamação/complicações
NF-kappa B/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipoproteins, LDL); 0 (NF-kappa B); 0 (TNFSF14 protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (oxidized low density lipoprotein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE


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[PMID]:28423548
[Au] Autor:Lee EH; Kim EM; Ji KY; Park AR; Choi HR; Lee HY; Kim SM; Chung BY; Park CH; Choi HJ; Ko YH; Bai HW; Kang HS
[Ad] Endereço:Research Division for Biotechnology, Advanced Radiation Technology Institute (ARTI), Korea Atomic Energy Insitute (KAERI), Jeongeup-si, Jeollabuk-do 580-185, Republic of Korea.
[Ti] Título:Axl acts as a tumor suppressor by regulating LIGHT expression in T lymphoma.
[So] Source:Oncotarget;8(13):20645-20655, 2017 Mar 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Axl is an oncogenic receptor tyrosine kinase that plays a role in many cancers. LIGHT (Lymphotoxin-related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells) is a ligand that induces robust anti-tumor immunity by enhancing the recruitment and activation of effector immune cells at tumor sites. We observed that mouse EL4 and human Jurkat T lymphoma cells that stably overexpressed Axl also showed high expression of LIGHT. When Jurkat-Axl cells were treated with Gas6, a ligand for Axl, LIGHT expression was upregulated through activation of the PI3K/AKT signaling pathway and transcriptional induction by Sp1. The lytic activity of cytotoxic T lymphocytes and natural killer cells was enhanced by EL4-Axl cells. In addition, tumor volume and growth were markedly reduced due to enhanced apoptotic cell death in EL4-Axl tumor-bearing mice as compared to control mice. We also observed upregulated expression of CCL5 and its receptor, CCR5, and enhanced intratumoral infiltration of cytotoxic T lymphocytes and natural killer cells in EL4-Axl-bearing mice as compared to mock controls. These data strongly suggested that Axl exerts novel tumor suppressor effects by inducing upregulation of LIGHT in the tumor microenvironment of T lymphoma.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica/fisiologia
Genes Supressores de Tumor/fisiologia
Linfoma de Células T/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Ensaio de Desvio de Mobilidade Eletroforética
Citometria de Fluxo
Imunofluorescência
Seres Humanos
Linfoma de Células T/patologia
Camundongos
Camundongos Endogâmicos C57BL
Mutagênese Sítio-Dirigida
Reação em Cadeia da Polimerase
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (axl receptor tyrosine kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15830


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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]:28249900
[Au] Autor:Qiao G; Qin J; Kunda N; Calata JF; Mahmud DL; Gann P; Fu YX; Rosenberg SA; Prabhakar BS; Maker AV
[Ad] Endereço:Department of Surgery, Division of Surgical Oncology, University of Illinois at Chicago, Chicago, Illinois.
[Ti] Título:LIGHT Elevation Enhances Immune Eradication of Colon Cancer Metastases.
[So] Source:Cancer Res;77(8):1880-1891, 2017 Apr 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The majority of patients with colon cancer will develop advanced disease, with the liver being the most common site of metastatic disease. Patients with increased numbers of tumor-infiltrating lymphocytes in primary colon tumors and liver metastases have improved outcomes. However, the molecular factors that could empower antitumor immune responses in this setting remain to be elucidated. We reported that the immunostimulatory cytokine LIGHT (TNFSF14) in the microenvironment of colon cancer metastases associates with improved patient survival, and here we demonstrate in an immunocompetent murine model that colon tumors expressing LIGHT stimulate lymphocyte proliferation and tumor cell-specific antitumor immune responses. In this model, increasing LIGHT expression in the microenvironment of either primary tumors or liver metastases triggered regression of established tumors and slowed the growth of liver metastases, driven by cytotoxic T-lymphocyte-mediated antitumor immunity. These responses corresponded with significant increases in tumor-infiltrating lymphocytes and increased expression of lymphocyte-homing signals in the metastatic tumors. Furthermore, we demonstrated evidence of durable tumor-specific antitumor immunity. In conclusion, increasing LIGHT expression increased T-cell proliferation, activation, and infiltration, resulting in enhanced tumor-specific immune-mediated tumor regressions in primary tumors and colorectal liver metastases. Mechanisms to increase LIGHT in the colon cancer microenvironment warrant further investigation and hold promise as an immunotherapeutic strategy. .
[Mh] Termos MeSH primário: Neoplasias do Colo/imunologia
Neoplasias do Colo/metabolismo
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/biossíntese
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Neoplasias do Colo/patologia
Feminino
Células HEK293
Seres Humanos
Neoplasias Hepáticas/imunologia
Neoplasias Hepáticas/secundário
Ativação Linfocitária
Linfócitos do Interstício Tumoral/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170510
[Lr] Data última revisão:
170510
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-1655


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[PMID]:28155222
[Au] Autor:Szczeklik W; Jakiela B; Wawrzycka-Adamczyk K; Sanak M; Hubalewska-Mazgaj M; Padjas A; Surmiak M; Szczeklik K; Sznajd J; Musial J
[Ad] Endereço:Department of Medicine, Jagiellonian University Medical College, Krakow, Poland.
[Ti] Título:Skewing toward Treg and Th2 responses is a characteristic feature of sustained remission in ANCA-positive granulomatosis with polyangiitis.
[So] Source:Eur J Immunol;47(4):724-733, 2017 Apr.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The objective of our study was to evaluate the T-helper (Th) and regulatory T (Treg) cell profile in ANCA-positive granulomatosis with polyangiitis (GPA) and its relation to disease activity. In a prospective study, we studied two groups of GPA patients: (i) disease flare (active-GPA, BVAS>6, n = 19), (ii) sustained remission (≥ 1-year prior enrollment, inactive-GPA, BVAS = 0, n = 18). 24 age-sex matched healthy subjects served as controls. Active-GPA patients were followed for 6 months and reevaluated during remission (early remission; n = 13). We analyzed subsets of Th-cells (flow cytometry), production of signature cytokines by in vitro stimulated lymphocytes, and broad spectrum of serum cytokines (Luminex). In all GPA patients we observed expansion of effector Th17 cells, and increased production of IL-17A by in vitro stimulated T cells, as compared to controls. Disease flare was characterized by marked reduction in Treg cells, whereas in sustained remission we showed expansion of both Treg and Th2 subset. Finally, analyzing the cytokine profile, we identified CCL23 and LIGHT, as potential biomarkers of active disease. We conclude that in GPA, expansion of Treg and Th2 lymphocytes in parallel to increased Th17 response is a characteristic feature of sustained remission. In contrast, Treg cells are markedly decreased in disease flare.
[Mh] Termos MeSH primário: Granulomatose com Poliangiite/imunologia
Linfócitos T Reguladores/imunologia
Células Th17/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Adulto
Anticorpos Anticitoplasma de Neutrófilos/sangue
Biomarcadores/metabolismo
Células Cultivadas
Quimiocinas CC/metabolismo
Estudos de Coortes
Progressão da Doença
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antineutrophil Cytoplasmic); 0 (Biomarkers); 0 (CCL23 protein, human); 0 (Chemokines, CC); 0 (TNFSF14 protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646810


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[PMID]:27864565
[Au] Autor:Maracle CX; Kucharzewska P; Helder B; van der Horst C; Correa de Sampaio P; Noort AR; van Zoest K; Griffioen AW; Olsson H; Tas SW
[Ad] Endereço:Amsterdam Rheumatology and immunology Center.
[Ti] Título:Targeting non-canonical nuclear factor-κB signalling attenuates neovascularization in a novel 3D model of rheumatoid arthritis synovial angiogenesis.
[So] Source:Rheumatology (Oxford);56(2):294-302, 2017 Feb.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Angiogenesis is crucial in RA disease progression. Lymphotoxin ß receptor (LTßR)-induced activation of the non-canonical nuclear factor-κB (NF-κB) pathway via NF-κB-inducing kinase (NIK) has been implicated in this process. Consequently, inhibition of this pathway may hold therapeutic potential in RA. We describe a novel three-dimensional (3D) model of synovial angiogenesis incorporating endothelial cells (ECs), RA fibroblast-like synoviocytes (RAFLSs) and RA synovial fluid (RASF) to further investigate the contributions of NF-κB in this process. METHODS: Spheroids consisting of RAFLSs and ECs were stimulated with RASF, the LTßR ligands LTß and LIGHT, or growth factor bFGF and VEGF, followed by quantification of EC sprouting using confocal microscopy and digital image analysis. Next, the effects of anginex, NIK-targeting siRNA (siNIK), LTßR-Ig fusion protein (baminercept) and a novel pharmacological NIK inhibitor were investigated. RESULTS: RASF significantly promoted sprout formation, which was blocked by the established angiogenesis inhibitor anginex (P < 0.05). LTß and LIGHT induced significant sprouting (P < 0.05), as did bFGF/VEGF (P < 0.01). siNIK pre-treatment of ECs led to reductions in LTßR-induced vessel formation (P < 0.05). LTßR-Ig not only blocked LTß- or LIGHT-induced sprouting, but also RASF-induced sprouting (P < 0.05). The NIK inhibitor blocked angiogenesis induced by LTß, LIGHT, growth factors (P < 0.05) and RASF (P < 0.01). CONCLUSION: We present a novel 3D model of synovial angiogenesis incorporating RAFLSs, ECs and RASF that mimics the in vivo situation. Using this system, we demonstrate that non-canonical NF-κB signalling promotes neovascularization and show that this model is useful for dissecting relative contributions of signalling pathways in specific cell types to angiogenic responses and for testing pharmacological inhibitors of angiogenesis.
[Mh] Termos MeSH primário: Células Endoteliais/efeitos dos fármacos
NF-kappa B/metabolismo
Neovascularização Patológica/metabolismo
Sinoviócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Artrite Reumatoide/metabolismo
Artrite Reumatoide/patologia
Células Cultivadas
Células Endoteliais/metabolismo
Células Endoteliais/patologia
Fatores de Crescimento de Fibroblastos/farmacologia
Seres Humanos
Receptor beta de Linfotoxina
Linfotoxina-beta/farmacologia
Microscopia Confocal
Neovascularização Patológica/patologia
Peptídeos/farmacologia
Proteínas Serina-Treonina Quinases/genética
RNA Interferente Pequeno
Proteínas Recombinantes de Fusão/farmacologia
Transdução de Sinais
Líquido Sinovial
Membrana Sinovial/metabolismo
Membrana Sinovial/patologia
Sinoviócitos/metabolismo
Sinoviócitos/patologia
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/farmacologia
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphotoxin beta Receptor); 0 (Lymphotoxin-beta); 0 (NF-kappa B); 0 (Peptides); 0 (RNA, Small Interfering); 0 (Recombinant Fusion Proteins); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (Vascular Endothelial Growth Factor A); 0 (anginex peptide); 0 (baminercept); 62031-54-3 (Fibroblast Growth Factors); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.25 (NF-kappa B kinase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161120
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kew393


  10 / 315 MEDLINE  
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[PMID]:27196595
[Au] Autor:Mejías-Luque R; Zöller J; Anderl F; Loew-Gil E; Vieth M; Adler T; Engler DB; Urban S; Browning JL; Müller A; Gerhard M; Heikenwalder M
[Ad] Endereço:Institut für Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universität München, Munich, Germany.
[Ti] Título:Lymphotoxin ß receptor signalling executes -driven gastric inflammation in a T4SS-dependent manner.
[So] Source:Gut;66(8):1369-1381, 2017 Aug.
[Is] ISSN:1468-3288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Lymphotoxin ß receptor (LTßR) signalling has been implicated in inflammation-associated tumour development in different tissues. We have analysed the role of LTßR and alternative NF-κB signalling in mediated gastric inflammation and pathology. DESIGN: We analysed several ligands and receptors of the alternative NF-κB pathway, RelB, p52 nuclear translocation and target genes in tissue samples of -infected patients with different degrees of gastritis or early gastric tumours by in situ hybridisation, immunohistochemistry, Western blot and real-time PCR analyses. Molecular mechanisms involved in LTßR activation by were assessed in vitro using human gastric cancer cell lines and distinct isolates. The effects of blocking or agonistically activating LTßR on gastric pathology during challenge with a human pathogenic strain were studied in a mouse model. RESULTS: Among the tested candidates, LT was significantly increased and activated alternative NF-κB signalling was observed in the gastric mucosa of -infected patients. induced LTßR-ligand expression in a type IV secretion system-dependent but CagA-independent manner, resulting in activation of the alternative NF-κB pathway, which was further enhanced by blocking canonical NF-κB during infection. Blocking LTßR signalling in vivo suppressed driven gastritis, whereas LTßR activation in gastric epithelial cells of infected mice induced a broadened pro-inflammatory chemokine milieu, resulting in exacerbated pathology. CONCLUSIONS: LTßR-triggered activation of alternative NF-κB signalling in gastric epithelial cells executes -induced chronic gastritis, representing a novel target to restrict gastric inflammation and pathology elicited by , while exclusively targeting canonical NF-κB may aggravate pathology by enhancing the alternative pathway.
[Mh] Termos MeSH primário: Quimiocinas/metabolismo
Gastrite/metabolismo
Infecções por Helicobacter/metabolismo
Helicobacter pylori
Receptor beta de Linfotoxina/metabolismo
NF-kappa B/metabolismo
Sistemas de Secreção Tipo IV/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Bactérias/metabolismo
Proteínas de Bactérias/metabolismo
Linhagem Celular Tumoral
Quimiocina CCL2/metabolismo
Quimiocina CCL20/metabolismo
Quimiocina CXCL10/metabolismo
Células Epiteliais/metabolismo
Feminino
Mucosa Gástrica/metabolismo
Gastrite/microbiologia
Infecções por Helicobacter/complicações
Seres Humanos
Receptor beta de Linfotoxina/antagonistas & inibidores
Receptor beta de Linfotoxina/genética
Camundongos
Camundongos Endogâmicos C57BL
RNA Mensageiro
Transdução de Sinais
Fator de Transcrição RelB/metabolismo
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Bacterial Proteins); 0 (Chemokine CCL2); 0 (Chemokine CCL20); 0 (Chemokine CXCL10); 0 (Chemokines); 0 (Lymphotoxin beta Receptor); 0 (NF-kappa B); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (Tumor Necrosis Factor-alpha); 0 (Type IV Secretion Systems); 0 (cagA protein, Helicobacter pylori); 147337-75-5 (Transcription Factor RelB)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.1136/gutjnl-2015-310783



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