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Pesquisa : D12.776.543.750.705.852.760.245 [Categoria DeCS]
Referências encontradas : 403 [refinar]
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[PMID]:28733031
[Au] Autor:Kim JS; Kim EJ; Kim HS; Kurie JM; Ahn YH
[Ad] Endereço:Department of Molecular Medicine and Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul 07985, South Korea.
[Ti] Título:MKK4 activates non-canonical NFκB signaling by promoting NFκB2-p100 processing.
[So] Source:Biochem Biophys Res Commun;491(2):337-342, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The NFκB family of transcription factors is crucial for innate or adaptive immunity, inflammation, and diseases including cancer. The two NFκB signaling pathways (canonical and non-canonical) differ from each other in extracellular signals, membrane receptors, signaling adaptors, and dimer subunits. The p52 (NFκB2) subunit, which participates in the non-canonical pathway, is generated by ubiquitin-mediated processing of the p100 precursor. Here, we found that NFκB2 processing and activation were mediated by mitogen-activated protein kinase kinase-4 (MKK4) and its substrate c-Jun N-terminal kinase (JNK). In MKK4-null mouse embryonic fibroblasts (MEFs), serum- and lymphotoxin ß receptor (LTßR) antibody-induced processing of p100 and nuclear translocation of p52 were found to be defective. Serum and LTßR antibody activated the MKK4-JNK signaling pathway, and SP600125, a JNK inhibitor, blocked p100 processing. Cellular senescence, one of the responses regulated by the non-canonical NFκB pathway, was observed more frequently in MKK4-null MEFs than in wildtype cells. These results suggest that the MKK4/JNK-dependent pathway regulates NFκB2 processing/activation and, through this mechanism, MKK4 and NFκB2 control cellular growth and senescence.
[Mh] Termos MeSH primário: Células Epiteliais/metabolismo
Fibroblastos/metabolismo
MAP Quinase Quinase 4/genética
Subunidade p52 de NF-kappa B/genética
[Mh] Termos MeSH secundário: Animais
Antracenos/farmacologia
Brônquios/citologia
Brônquios/metabolismo
Linhagem Celular
Linhagem Celular Tumoral
Proliferação Celular
Senescência Celular
Células Epiteliais/citologia
Fibroblastos/citologia
Regulação da Expressão Gênica
Seres Humanos
Receptor beta de Linfotoxina/genética
Receptor beta de Linfotoxina/metabolismo
MAP Quinase Quinase 4/antagonistas & inibidores
MAP Quinase Quinase 4/metabolismo
Camundongos
Subunidade p52 de NF-kappa B/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthracenes); 0 (LTBR protein, human); 0 (Lymphotoxin beta Receptor); 0 (NF-kappa B p52 Subunit); 0 (NFKB2 protein, human); 0 (Protein Kinase Inhibitors); 1TW30Y2766 (pyrazolanthrone); EC 2.7.12.2 (MAP Kinase Kinase 4); EC 2.7.12.2 (MAP2K4 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE


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[PMID]:28709801
[Au] Autor:Onder L; Mörbe U; Pikor N; Novkovic M; Cheng HW; Hehlgans T; Pfeffer K; Becher B; Waisman A; Rülicke T; Gommerman J; Mueller CG; Sawa S; Scandella E; Ludewig B
[Ad] Endereço:Institute of Immunobiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
[Ti] Título:Lymphatic Endothelial Cells Control Initiation of Lymph Node Organogenesis.
[So] Source:Immunity;47(1):80-92.e4, 2017 Jul 18.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lymph nodes (LNs) are strategically situated throughout the body at junctures of the blood vascular and lymphatic systems to direct immune responses against antigens draining from peripheral tissues. The current paradigm describes LN development as a programmed process that is governed through the interaction between mesenchymal lymphoid tissue organizer (LTo) cells and hematopoietic lymphoid tissue inducer (LTi) cells. Using cell-type-specific ablation of key molecules involved in lymphoid organogenesis, we found that initiation of LN development is dependent on LTi-cell-mediated activation of lymphatic endothelial cells (LECs) and that engagement of mesenchymal stromal cells is a succeeding event. LEC activation was mediated mainly by signaling through receptor activator of NF-κB (RANK) and the non-canonical NF-κB pathway and was steered by sphingosine-1-phosphate-receptor-dependent retention of LTi cells in the LN anlage. Finally, the finding that pharmacologically enforced interaction between LTi cells and LECs promotes ectopic LN formation underscores the central LTo function of LECs.
[Mh] Termos MeSH primário: Células Endoteliais/fisiologia
Linfonodos/fisiologia
Células Mesenquimais Estromais/fisiologia
Organogênese
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Coristoma
Embrião de Mamíferos
Receptor beta de Linfotoxina/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
NF-kappa B/metabolismo
Receptor Ativador de Fator Nuclear kappa-B/metabolismo
Receptores de Lisoesfingolipídeo/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ltbr protein, mouse); 0 (Lymphotoxin beta Receptor); 0 (NF-kappa B); 0 (Receptor Activator of Nuclear Factor-kappa B); 0 (Receptors, Lysosphingolipid); 0 (Tnfrsf11a protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


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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


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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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[PMID]:27936003
[Au] Autor:Milicevic NM; Nohroudi K; Schmidt F; Schmidt H; Ringer C; Sorensen GL; Milicevic Z; Westermann J
[Ad] Endereço:Institute of Histology and Embryology, Faculty of Medicine, University of Beograd, Beograd, Serbia.
[Ti] Título:Growth of Murine Splenic Tissue Is Suppressed by Lymphotoxin ß-Receptor Signaling (LTßR) Originating from Splenic and Non-Splenic Tissues.
[So] Source:PLoS One;11(12):e0166901, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Development and maintenance of secondary lymphoid organs such as lymph nodes and spleen essentially depend on lymphotoxin ß-receptor (LTßR) signaling. It is unclear, however, by which molecular mechanism their size is limited. Here, we investigate whether the LTßR pathway is also growth suppressing. By using splenic tissue transplantation it is possible to analyze a potential contribution of LTßR signaling inside and outside of the implanted tissue. We show that LTßR signaling within the endogenous spleen and within non-splenic tissues both significantly suppressed the regeneration of implanted splenic tissue. The suppressive activity positively correlated with the total number of LTßR expressing cells in the animal (regenerate weights of 115 ± 8 mg in LTßR deficient recipients and of 12 ± 9 mg in wild-type recipients), affected also developed splenic tissue, and was induced but not executed via LTßR signaling. Two-dimensional differential gel electrophoresis and subsequent mass spectrometry of stromal splenic tissue was applied to screen for potential factors mediating the LTßR dependent suppressive activity. Thus, LTßR dependent growth suppression is involved in regulating the size of secondary lymphoid organs, and might be therapeutically used to eradicate tertiary lymphoid tissues during autoimmune diseases.
[Mh] Termos MeSH primário: Receptor beta de Linfotoxina/metabolismo
Transdução de Sinais
Baço/metabolismo
Transplante de Tecidos/métodos
[Mh] Termos MeSH secundário: Animais
Western Blotting
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Quimiocina CCL19/genética
Quimiocina CCL19/metabolismo
Quimiocina CCL21/genética
Quimiocina CCL21/metabolismo
Eletroforese em Gel Bidimensional
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Expressão Gênica
Glicoproteínas/genética
Glicoproteínas/metabolismo
Interleucina-17/genética
Interleucina-17/metabolismo
Receptor beta de Linfotoxina/genética
Espectrometria de Massas
Camundongos Endogâmicos C57BL
Camundongos Knockout
Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/genética
Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/metabolismo
Regeneração
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Baço/crescimento & desenvolvimento
Baço/transplante
Esplenectomia
Células Estromais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Chemokine CCL19); 0 (Chemokine CCL21); 0 (Extracellular Matrix Proteins); 0 (Glycoproteins); 0 (Interleukin-17); 0 (Lymphotoxin beta Receptor); 0 (MFAP4 protein, mouse); 0 (Nuclear Receptor Subfamily 1, Group F, Member 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161210
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0166901


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[PMID]:27835685
[Au] Autor:Heo SK; Noh EK; Gwon GD; Kim JY; Jo JC; Choi Y; Koh S; Baek JH; Min YJ; Kim H
[Ad] Endereço:Biomedical Research Center, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 682-060, Republic of Korea.
[Ti] Título:LIGHT (TNFSF14) Increases the Survival and Proliferation of Human Bone Marrow-Derived Mesenchymal Stem Cells.
[So] Source:PLoS One;11(11):e0166589, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:LIGHT (HVEM-L, TNFSF14, or CD258), an entity homologous to lymphotoxins, with inducible nature and the ability to compete with herpes simplex virus glycoprotein D for herpes virus entry mediator (HVEM)/tumor necrosis factor (TNF)-related 2, is a member of the TNF superfamily. It is expressed as a homotrimer on activated T cells and dendritic cells (DCs), and has three receptors: HVEM, LT-ß receptor (LTßR), and decoy receptor 3 (DcR3). So far, three receptors with distinct cellular expression patterns are known to interact with LIGHT. Follicular DCs and stromal cells bind LIGHT through LTßR. We monitored the effects of LIGHT on human bone marrow-derived mesenchymal stem cells (BM-MSCs). At first, we checked the negative and positive differentiation markers of BM-MSCs. And we confirmed the quality of MSCs by staining cells undergoing adipogenesis (Oil Red O staining), chondrogenesis (Alcian blue staining), and osteogenesis (Alizarin red staining). After rhLIGHT treatment, we monitored the count, viability, and proliferation of cells and cell cycle distribution. PDGF and TGFß production by rhLIGHT was examined by ELISA, and the underlying biological mechanisms were studied by immunoblotting by rhLIGHT treatment. LTßR was constitutively expressed on the surface of human BM-MSCs. Cell number and viability increased after rhLIGHT treatment. BM-MSC proliferation was induced by an increase in the S/G2/M phase. The expression of not only diverse cyclins such as cyclin B1, D1, D3, and E, but also CDK1 and CDK2, increased, while that of p27 decreased, after rhLIGHT treatment. RhLIGHT-induced PDGF and TGFß production mediated by STAT3 and Smad3 activation accelerated BM-MSC proliferation. Thus, LIGHT and LTßR interaction increases the survival and proliferation of human BM-MSCs, and therefore, LIGHT might play an important role in stem cell therapy.
[Mh] Termos MeSH primário: Células da Medula Óssea/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Receptor beta de Linfotoxina/genética
Células Mesenquimais Estromais/efeitos dos fármacos
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/farmacologia
[Mh] Termos MeSH secundário: Adipócitos/citologia
Adipócitos/efeitos dos fármacos
Adipócitos/metabolismo
Células da Medula Óssea/citologia
Células da Medula Óssea/metabolismo
Proteína Quinase CDC2
Ciclo Celular
Diferenciação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Condrócitos/citologia
Condrócitos/efeitos dos fármacos
Condrócitos/metabolismo
Quinase 2 Dependente de Ciclina/genética
Quinase 2 Dependente de Ciclina/metabolismo
Inibidor de Quinase Dependente de Ciclina p27/genética
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Quinases Ciclina-Dependentes/genética
Quinases Ciclina-Dependentes/metabolismo
Ciclinas/genética
Ciclinas/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Receptor beta de Linfotoxina/metabolismo
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/metabolismo
Análise em Microsséries
Osteócitos/citologia
Osteócitos/efeitos dos fármacos
Osteócitos/metabolismo
Fator de Crescimento Derivado de Plaquetas/genética
Fator de Crescimento Derivado de Plaquetas/metabolismo
Cultura Primária de Células
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteínas Recombinantes/farmacologia
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Proteína Smad3/genética
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclins); 0 (LTBR protein, human); 0 (Lymphotoxin beta Receptor); 0 (Platelet-Derived Growth Factor); 0 (Recombinant Proteins); 0 (SMAD3 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Smad3 Protein); 0 (TNFSF14 protein, human); 0 (Transforming Growth Factor beta); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (platelet-derived growth factor A); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.7.11.22 (CDC2 Protein Kinase); EC 2.7.11.22 (CDK1 protein, human); EC 2.7.11.22 (CDK2 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 2); EC 2.7.11.22 (Cyclin-Dependent Kinases)
[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:161112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0166589


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[PMID]:27820602
[Au] Autor:Inoue M; Chen PH; Siecinski S; Li QJ; Liu C; Steinman L; Gregory SG; Benner E; Shinohara ML
[Ad] Endereço:Department of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
[Ti] Título:An interferon-ß-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage.
[So] Source:Nat Neurosci;19(12):1599-1609, 2016 Dec.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation induced by innate immunity influences the development of T cell-mediated autoimmunity in multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). We found that strong activation of innate immunity induced Nod-like receptor protein 3 (NLRP3) inflammasome-independent and interferon-ß (IFNß)-resistant EAE (termed type B EAE), whereas EAE induced by weak activation of innate immunity requires the NLRP3 inflammasome and is sensitive to IFNß treatment. Instead, an alternative inflammatory mechanism, including membrane-bound lymphotoxin-ß receptor (LTßR) and CXC chemokine receptor 2 (CXCR2), is involved in type B EAE development, and type B EAE is ameliorated by antagonizing these receptors. Relative expression of Ltbr and Cxcr2 genes was indeed enhanced in patients with IFNß-resistant multiple sclerosis. Remission was minimal in type B EAE due to neuronal damages induced by semaphorin 6B upregulation on CD4 T cells. Our data reveal a new inflammatory mechanism by which an IFNß-resistant EAE subtype develops.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental
Interferon beta/imunologia
Receptor beta de Linfotoxina/genética
Proteína 3 que Contém Domínio de Pirina da Família NLR/genética
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central/imunologia
Sistema Nervoso Central/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/genética
Encefalomielite Autoimune Experimental/imunologia
Seres Humanos
Imunidade Inata/genética
Imunidade Inata/imunologia
Inflamassomos/genética
Inflamassomos/imunologia
Interferon beta/genética
Camundongos Knockout
Esclerose Múltipla/genética
Esclerose Múltipla/imunologia
Receptores de Interleucina-8B/genética
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammasomes); 0 (LTBR protein, human); 0 (Ltbr protein, mouse); 0 (Lymphotoxin beta Receptor); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP3 protein, human); 0 (Nlrp3 protein, mouse); 0 (Receptors, Interleukin-8B); 77238-31-4 (Interferon-beta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4421


  8 / 403 MEDLINE  
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[PMID]:27815440
[Au] Autor:Haskett S; Ding J; Zhang W; Thai A; Cullen P; Xu S; Petersen B; Kuznetsov G; Jandreski L; Hamann S; Reynolds TL; Allaire N; Zheng TS; Mingueneau M
[Ad] Endereço:Immunology Research, Biogen, Cambridge, MA 02142.
[Ti] Título:Identification of Novel CD4+ T Cell Subsets in the Target Tissue of Sjögren's Syndrome and Their Differential Regulation by the Lymphotoxin/LIGHT Signaling Axis.
[So] Source:J Immunol;197(10):3806-3819, 2016 Nov 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite being one of the most common rheumatologic diseases, there is still no disease-modifying drug for primary Sjögren's syndrome (pSS). Advancing our knowledge of the target tissue has been limited by the low dimensionality of histology techniques and the small size of human salivary gland biopsies. In this study, we took advantage of a molecularly validated mouse model of pSS to characterize tissue-infiltrating CD4 T cells and their regulation by the lymphotoxin/LIGHT signaling axis. Novel cell subsets were identified by combining highly dimensional flow and mass cytometry with transcriptomic analyses. Pharmacologic modulation of the LTßR signaling pathway was achieved by treating mice with LTßR-Ig, a therapeutic intervention currently being tested in pSS patients (Baminercept trial NCT01552681). Using these approaches, we identified two novel CD4 T cell subsets characterized by high levels of PD1: Prdm1 effector regulatory T cells expressing immunoregulatory factors, such as Il10, Areg, Fgl2, and Itgb8, and Il21 effector conventional T cells expressing a pathogenic transcriptional signature. Mirroring these observations in mice, large numbers of CD4 PD1 T cells were detected in salivary glands from Sjögren's patients but not in normal salivary glands or kidney biopsies from lupus nephritis patients. Unexpectedly, LTßR-Ig selectively halted the recruitment of PD1 naive, but not PD1 , effector T cells to the target tissue, leaving the cells with pathogenic potential unaffected. Altogether, this study revealed new cellular players in pSS pathogenesis, their transcriptional signatures, and differential dependency on the lymphotoxin/LIGHT signaling axis that help to interpret the negative results of the Baminercept trial and will guide future therapeutic interventions.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Receptor beta de Linfotoxina/metabolismo
Linfotoxina-alfa/metabolismo
Glândulas Salivares/imunologia
Síndrome de Sjogren/imunologia
Síndrome de Sjogren/fisiopatologia
Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Anfirregulina/genética
Animais
Biópsia
Ensaios Clínicos como Assunto
Modelos Animais de Doenças
Citometria de Fluxo
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Seres Humanos
Interleucina-10/genética
Interleucinas/genética
Rim/patologia
Nefrite Lúpica/imunologia
Linfotoxina-alfa/genética
Camundongos
Glândulas Salivares/patologia
Transdução de Sinais
Síndrome de Sjogren/terapia
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amphiregulin); 0 (Areg protein, mouse); 0 (IL10 protein, mouse); 0 (Interleukins); 0 (Lymphotoxin beta Receptor); 0 (Lymphotoxin-alpha); 0 (Tnfsf14 protein, mouse); 0 (Tumor Necrosis Factor Ligand Superfamily Member 14); 0 (interleukin-21); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


  9 / 403 MEDLINE  
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[PMID]:27706556
[Au] Autor:Xia RW; Sun L; Qin WY; Gan LN; Bao WB; Wu SL
[Ad] Endereço:Key Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design of Jiangsu Province, College of Animal Science and Technology, Yangzhou University, Jiangsu Yangzhou, China.
[Ti] Título:Developmental expression of LTßR and differential expression in Escherichia coli F18 resistant/sensitive piglets.
[So] Source:Genet Mol Res;15(3), 2016 Aug 19.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:We analyzed LTßR mRNA expression in piglets from birth to weaning and compared the differential expression between Escherichia coli F18-resistant and sensitive populations to determine whether this gene could be used as a genetic marker for E. coli F18 resistance. Sutai piglets of different age groups (8, 18, 30, and 35 days; N = 4 each) and piglets demonstrating resistance/sensitivity to E. coli F18 were used. LTßR expression levels were determined by real-time PCR. The LTßR expression levels in the lymph node, duodenum, and jejunum were significantly higher in 8-day-old piglets than in the other age groups (P < 0.01), and the expression levels were significantly higher in the lungs of 8-day-old piglets than in 35-day-old piglets (P < 0.01) and 30 day-old piglets (P < 0.05). In liver tissue, the expression level was significantly higher in the 35-day-old piglets than in other age groups (P < 0.01). In the stomach tissue, the expression level was significantly higher in 35-day-old piglets than in 18-day-old piglets (P < 0.05). LTßR expression in the lymph nodes was significantly higher in the resistant group than in the sensitive group (P < 0.01), but there was no significant difference in the other tissues (P > 0.05). These results indicate that 8 days after birth is a crucial stage in the formation of mesentery lymph nodes and immune barriers in pigs, and increased expression of LTßR may be beneficial for developing resistance to E. coli F18.
[Mh] Termos MeSH primário: Infecções por Escherichia coli/veterinária
Receptor beta de Linfotoxina/biossíntese
Doenças dos Suínos/patologia
Suínos/genética
[Mh] Termos MeSH secundário: Animais
Peptídeos Catiônicos Antimicrobianos/biossíntese
Peptídeos Catiônicos Antimicrobianos/genética
Biomarcadores
Resistência à Doença
Duodeno/metabolismo
Escherichia coli/fisiologia
Infecções por Escherichia coli/genética
Expressão Gênica
Jejuno/metabolismo
Receptor beta de Linfotoxina/genética
Doenças dos Suínos/genética
Doenças dos Suínos/microbiologia
Desmame
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (Biomarkers); 0 (Lymphotoxin beta Receptor)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE
[do] DOI:10.4238/gmr.15038377


  10 / 403 MEDLINE  
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[PMID]:27549174
[Au] Autor:Lucas B; James KD; Cosway EJ; Parnell SM; Tumanov AV; Ware CF; Jenkinson WE; Anderson G
[Ad] Endereço:Medical Research Council Centre for Immune Regulation, Institute for Immunology and Immunotherapy, University of Birmingham, Birmingham B15 2TT, United Kingdom;
[Ti] Título:Lymphotoxin ß Receptor Controls T Cell Progenitor Entry to the Thymus.
[So] Source:J Immunol;197(7):2665-72, 2016 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The recruitment of lymphoid progenitors to the thymus is essential to sustain T cell production throughout life. Importantly, it also limits T lineage regeneration following bone marrow transplantation, and so contributes to the secondary immunodeficiency that is caused by delayed immune reconstitution. Despite this significance, the mechanisms that control thymus colonization are poorly understood. In this study, we show that in both the steady-state and after bone marrow transplant, lymphotoxin ß receptor (LTßR) controls entry of T cell progenitors to the thymus. We show that this requirement maps to thymic stroma, further underlining the key importance of this TNFR superfamily member in regulation of thymic microenvironments. Importantly, analysis of the requirement for LTßR in relationship to known regulators of thymus seeding suggests that it acts independently of its regulation of thymus-homing chemokines. Rather, we show that LTßR differentially regulates intrathymic expression of adhesion molecules known to play a role in T cell progenitor entry to the thymus. Finally, Ab-mediated in vivo LTßR stimulation following bone marrow transplant enhances initial thymus recovery and boosts donor-derived T cell numbers, which correlates with increased adhesion molecule expression by thymic stroma. Collectively, we reveal a novel link between LTßR and thymic stromal cells in thymus colonization, and highlight its potential as an immunotherapeutic target to boost T cell reconstitution after transplantation.
[Mh] Termos MeSH primário: Movimento Celular
Receptor beta de Linfotoxina/imunologia
Células-Tronco/citologia
Linfócitos T/citologia
Timo/citologia
[Mh] Termos MeSH secundário: Animais
Receptor beta de Linfotoxina/deficiência
Camundongos
Camundongos Congênicos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células-Tronco/imunologia
Linfócitos T/imunologia
Timo/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lymphotoxin beta Receptor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160824
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601189



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