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


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[PMID]:28410993
[Au] Autor:Gupta JC; Hada RS; Sahai P; Talwar GP
[Ad] Endereço:Talwar Research Foundation, E-8 Neb Valley, New Delhi 110068, India. Electronic address: jcgupta@outlook.com.
[Ti] Título:Development of a novel recombinant LHRH fusion protein for therapy of androgen and estrogen dependent cancers.
[So] Source:Protein Expr Purif;134:132-138, 2017 Jun.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:LHRH based vaccines are promising candidates for therapy of androgen and estrogen dependent cancers. We report in this communication development of a novel recombinant protein vaccine candidate against LHRH. A synthetic gene was designed in which the codon sequence in the LHRH decapeptide was modified by substituting the codon for 6-glycine with that of l-leucine. Further the LHRH(6leu) gene was linked to heat-labile enterotoxin of E. coli (LTB) as carrier. This LHRH(6leu)-LTB gene was cloned into a prokaryotic expression vector under the control of inducible and strong bacteriophage T7 promoter to over-express LHRH(leu) fused to LTB as recombinant protein in E. coli. Recombinant LHRH(leu)-LTB protein of ∼14 kDa size, was purified from inclusion bodies using in-situ refolding on the column and Ni-NTA based immobilized affinity chromatography. Western blot confirmed the immunoreactivity of purified LHRH(leu)-LTB fusion protein with anti-LHRH monoclonal antibody. The vaccine protein was further characterized by mass spectroscopy, circular dichroism and fluorescence spectroscopy. This communication reports a recombinant LHRH fusion protein with potential for blocking of sex hormones production for eventual therapy of sex hormones dependent neoplasms.
[Mh] Termos MeSH primário: Androgênios
Vacinas Anticâncer
Estrogênios
Hormônio Liberador de Gonadotropina
Linfotoxina-beta
Neoplasias/terapia
Proteínas Recombinantes de Fusão
[Mh] Termos MeSH secundário: Vacinas Anticâncer/biossíntese
Vacinas Anticâncer/genética
Vacinas Anticâncer/uso terapêutico
Hormônio Liberador de Gonadotropina/biossíntese
Hormônio Liberador de Gonadotropina/genética
Hormônio Liberador de Gonadotropina/uso terapêutico
Seres Humanos
Linfotoxina-beta/biossíntese
Linfotoxina-beta/uso terapêutico
Proteínas Recombinantes de Fusão/biossíntese
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (Cancer Vaccines); 0 (Estrogens); 0 (LTB protein, human); 0 (Lymphotoxin-beta); 0 (Recombinant Fusion Proteins); 33515-09-2 (Gonadotropin-Releasing Hormone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170416
[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]:27098405
[Au] Autor:Ciccia F; Rizzo A; Maugeri R; Alessandro R; Croci S; Guggino G; Cavazza A; Raimondo S; Cannizzaro A; Iacopino DG; Salvarani C; Triolo G
[Ad] Endereço:Dipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, Università degli Studi di Palermo, Palermo, Italy.
[Ti] Título:Ectopic expression of CXCL13, BAFF, APRIL and LT-ß is associated with artery tertiary lymphoid organs in giant cell arteritis.
[So] Source:Ann Rheum Dis;76(1):235-243, 2017 Jan.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To investigate whether artery tertiary lymphoid organs (ATLOs) are present in giant cell arteritis (GCA) and that their formation is associated with the ectopic expression of constitutive lymphoid tissue-homing chemokines. METHODS: Reverse transcriptase PCR, immunohistochemical and immunofluorescence analysis were used to determine the presence of ectopic ATLOs in GCA and the expression of chemokines/chemokine receptors and cytokines involved in lymphoneogenesis in the temporal artery samples obtained from 50 patients with GCA and 30 controls. The presence of lymphatic conduits, of follicular dendritic cells (FDCs) precursors and lymphoid tissue inducer cells was also investigated. Finally, expression of CXCL13, B cell activating factor (BAFF), a proliferation-inducing ligand (APRIL) and CCL21 by isolated myofibroblasts was evaluated before and after stimulation with Toll-like receptors (TLRs) agonists and cytokines. RESULTS: ATLOs were observed in the media layer of 60% of patients with GCA in close proximity to high endothelial venules and independently by the age of patients and the presence of atherosclerosis. ATLO formation was also accompanied by the expression of CXCL13, BAFF, a proliferation-inducing ligand (APRIL), lymphotoxin (LT)-ß, interleukin (IL)-17 and IL-7, the presence of FDC precursors and of lymphoid conduits. Stimulation of myofibroblasts with TLR agonists and cytokines resulted in the upregulation of BAFF and CXCL13. CONCLUSIONS: ATLOs occur in the inflamed arteries of patients with GCA possibly representing the immune sites where immune responses towards unknown arterial wall-derived antigens may be organised.
[Mh] Termos MeSH primário: Quimiocinas/metabolismo
Expressão Ectópica do Gene/imunologia
Arterite de Células Gigantes/imunologia
Estruturas Linfoides Terciárias/imunologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Fator Ativador de Células B/metabolismo
Biópsia
Células Cultivadas
Quimiocina CXCL13/metabolismo
Citocinas/metabolismo
Feminino
Arterite de Células Gigantes/complicações
Arterite de Células Gigantes/patologia
Seres Humanos
Linfotoxina-beta/metabolismo
Masculino
Meia-Idade
Miofibroblastos/metabolismo
Receptores de Quimiocinas/metabolismo
Artérias Temporais/patologia
Estruturas Linfoides Terciárias/etiologia
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (CXCL13 protein, human); 0 (Chemokine CXCL13); 0 (Chemokines); 0 (Cytokines); 0 (LTB protein, human); 0 (Lymphotoxin-beta); 0 (Receptors, Chemokine); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170530
[Lr] Data última revisão:
170530
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-209217


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[PMID]:27721238
[Au] Autor:Chia JJ; Zhu T; Chyou S; Dasoveanu DC; Carballo C; Tian S; Magro CM; Rodeo S; Spiera RF; Ruddle NH; McGraw TE; Browning JL; Lafyatis R; Gordon JK; Lu TT
[Ti] Título:Dendritic cells maintain dermal adipose-derived stromal cells in skin fibrosis.
[So] Source:J Clin Invest;126(11):4331-4345, 2016 Nov 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Scleroderma is a group of skin-fibrosing diseases for which there are no effective treatments. A feature of the skin fibrosis typical of scleroderma is atrophy of the dermal white adipose tissue (DWAT). Adipose tissue contains adipose-derived mesenchymal stromal cells (ADSCs) that have regenerative and reparative functions; however, whether DWAT atrophy in fibrosis is accompanied by ADSC loss is poorly understood, as are the mechanisms that might maintain ADSC survival in fibrotic skin. Here, we have shown that DWAT ADSC numbers were reduced, likely because of cell death, in 2 murine models of scleroderma skin fibrosis. The remaining ADSCs showed a partial dependence on dendritic cells (DCs) for survival. Lymphotoxin ß (LTß) expression in DCs maintained ADSC survival in fibrotic skin by activating an LTß receptor/ß1 integrin (LTßR/ß1 integrin) pathway on ADSCs. Stimulation of LTßR augmented the engraftment of therapeutically injected ADSCs, which was associated with reductions in skin fibrosis and improved skin function. These findings provide insight into the effects of skin fibrosis on DWAT ADSCs, identify a DC-ADSC survival axis in fibrotic skin, and suggest an approach for improving mesenchymal stromal cell therapy in scleroderma and other diseases.
[Mh] Termos MeSH primário: Células Dendríticas/metabolismo
Derme/metabolismo
Esclerodermia Difusa/metabolismo
Gordura Subcutânea/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/genética
Células Dendríticas/patologia
Derme/patologia
Modelos Animais de Doenças
Feminino
Fibrose
Integrina beta1/genética
Integrina beta1/metabolismo
Linfotoxina-beta/genética
Linfotoxina-beta/metabolismo
Camundongos
Camundongos Knockout
Esclerodermia Difusa/genética
Esclerodermia Difusa/patologia
Células Estromais/metabolismo
Células Estromais/patologia
Gordura Subcutânea/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin beta1); 0 (Ltb protein, mouse); 0 (Lymphotoxin-beta)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


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[PMID]:27478039
[Au] Autor:Endig J; Buitrago-Molina LE; Marhenke S; Reisinger F; Saborowski A; Schütt J; Limbourg F; Könecke C; Schreder A; Michael A; Misslitz AC; Healy ME; Geffers R; Clavel T; Haller D; Unger K; Finegold M; Weber A; Manns MP; Longerich T; Heikenwälder M; Vogel A
[Ad] Endereço:Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, 30625 Hannover, Germany.
[Ti] Título:Dual Role of the Adaptive Immune System in Liver Injury and Hepatocellular Carcinoma Development.
[So] Source:Cancer Cell;30(2):308-323, 2016 Aug 08.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) represents a classic example of inflammation-linked cancer. To characterize the role of the immune system in hepatic injury and tumor development, we comparatively studied the extent of liver disease and hepatocarcinogenesis in immunocompromised versus immunocompetent Fah-deficient mice. Strikingly, chronic liver injury and tumor development were markedly suppressed in alymphoid Fah(-/-) mice despite an overall increased mortality. Mechanistically, we show that CD8(+) T cells and lymphotoxin ß are central mediators of HCC formation. Antibody-mediated depletion of CD8(+) T cells as well as pharmacological inhibition of the lymphotoxin-ß receptor markedly delays tumor development in mice with chronic liver injury. Thus, our study unveils distinct functions of the immune system, which are required for liver regeneration, survival, and hepatocarcinogenesis.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/imunologia
Hepatopatias/imunologia
Neoplasias Hepáticas/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Carcinogênese/imunologia
Carcinoma Hepatocelular/patologia
Seres Humanos
Hidrolases/imunologia
Hepatopatias/patologia
Neoplasias Hepáticas/patologia
Regeneração Hepática/imunologia
Linfotoxina-beta/imunologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LTB protein, human); 0 (Ltb protein, mouse); 0 (Lymphotoxin-beta); EC 3.- (Hydrolases); EC 3.7.1.2 (fumarylacetoacetase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160802
[St] Status:MEDLINE


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[PMID]:27010197
[Au] Autor:Cordeiro OG; Chypre M; Brouard N; Rauber S; Alloush F; Romera-Hernandez M; Bénézech C; Li Z; Eckly A; Coles MC; Rot A; Yagita H; Léon C; Ludewig B; Cupedo T; Lanza F; Mueller CG
[Ad] Endereço:CNRS UPR 3572, University of Strasbourg, Laboratory of Immunopathology and Therapeutic Chemistry/ MEDALIS, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
[Ti] Título:Integrin-Alpha IIb Identifies Murine Lymph Node Lymphatic Endothelial Cells Responsive to RANKL.
[So] Source:PLoS One;11(3):e0151848, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microenvironment and activation signals likely imprint heterogeneity in the lymphatic endothelial cell (LEC) population. Particularly LECs of secondary lymphoid organs are exposed to different cell types and immune stimuli. However, our understanding of the nature of LEC activation signals and their cell source within the secondary lymphoid organ in the steady state remains incomplete. Here we show that integrin alpha 2b (ITGA2b), known to be carried by platelets, megakaryocytes and hematopoietic progenitors, is expressed by a lymph node subset of LECs, residing in medullary, cortical and subcapsular sinuses. In the subcapsular sinus, the floor but not the ceiling layer expresses the integrin, being excluded from ACKR4+ LECs but overlapping with MAdCAM-1 expression. ITGA2b expression increases in response to immunization, raising the possibility that heterogeneous ITGA2b levels reflect variation in exposure to activation signals. We show that alterations of the level of receptor activator of NF-κB ligand (RANKL), by overexpression, neutralization or deletion from stromal marginal reticular cells, affected the proportion of ITGA2b+ LECs. Lymph node LECs but not peripheral LECs express RANK. In addition, we found that lymphotoxin-ß receptor signaling likewise regulated the proportion of ITGA2b+ LECs. These findings demonstrate that stromal reticular cells activate LECs via RANKL and support the action of hematopoietic cell-derived lymphotoxin.
[Mh] Termos MeSH primário: Células Endoteliais/imunologia
Linfonodos/citologia
Glicoproteína IIb da Membrana de Plaquetas/imunologia
Ligante RANK/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Células Endoteliais/citologia
Fibronectinas/imunologia
Linfonodos/imunologia
Linfotoxina-beta/imunologia
Camundongos Endogâmicos C57BL
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fibronectins); 0 (Lymphotoxin-beta); 0 (Platelet Membrane Glycoprotein IIb); 0 (RANK Ligand); 0 (Tnfsf11 protein, mouse)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160325
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0151848


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[PMID]:26874227
[Au] Autor:Donovan GM; Lythe G
[Ad] Endereço:Department of Mathematics, University of Auckland, Private Bag 92019, Auckland, New Zealand. Electronic address: g.donovan@auckland.ac.nz.
[Ti] Título:T cell and reticular network co-dependence in HIV infection.
[So] Source:J Theor Biol;395:211-220, 2016 Apr 21.
[Is] ISSN:1095-8541
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fibroblastic reticular cells (FRC) are arranged on a network in the T cell zone of lymph nodes, forming a scaffold for T cell migration, and providing survival factors, especially interleukin-7 (IL-7). Conversely, CD4(+) T cells are the major producers of lymphotoxin-ß (LT-ß), necessary for the construction and maintenance of the FRC network. This interdependence creates the possibility of a vicious cycle, perpetuating loss of both FRC and T cells. Furthermore, evidence that HIV infection is responsible for collagenation of the network suggests that long term loss of network function might be responsible for the attenuated recovery in T cell count seen in HIV patients undergoing antiretroviral therapy (ART). We present computational and mathematical models of this interaction mechanism and subsequent naive CD4(+) T-cell depletion in which (1) collagen deposition impedes access of naive T cells to IL-7 on the FRC and loss of IL-7 production by loss of FRC network itself, leading to the depletion of naive T cells through increased apoptosis; and (2) depletion of naive T cells as the source of LT-ß on which the FRC depend for survival leads to loss of the network, thereby amplifying and perpetuating the cycle of depletion of both naive T cells and stromal cells. Our computational model explicitly includes an FRC network and its cytokine exchange with a heterogeneous T-cell population. We also derive lumped models, in terms of partial differential equations and reduced to ordinary differential equations, that provide additional insight into the mechanisms at work. The central conclusions are that (1) damage to the reticular network, caused by HIV infection is a plausible mechanism for attenuated recovery post-ART; (2) within this, the production of T cell survival factors by FRCs may be the key rate-limiting step; and (3) the methods of model reduction and analysis presented are useful for both immunological studies and other contexts in which agent-based models are severely limited by computational cost.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Fibroblastos/imunologia
Infecções por HIV/imunologia
Linfonodos/imunologia
Modelos Imunológicos
[Mh] Termos MeSH secundário: Antirretrovirais/uso terapêutico
Infecções por HIV/tratamento farmacológico
Seres Humanos
Interleucina-7/imunologia
Linfotoxina-beta/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Retroviral Agents); 0 (IL7 protein, human); 0 (Interleukin-7); 0 (Lymphotoxin-beta)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170725
[Lr] Data última revisão:
170725
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160214
[St] Status:MEDLINE


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[PMID]:26553386
[Au] Autor:Shaabani N; Khairnar V; Duhan V; Zhou F; Tur RF; Häussinger D; Recher M; Tumanov AV; Hardt C; Pinschewer D; Christen U; Lang PA; Honke N; Lang KS
[Ad] Endereço:Institute of Immunology, Faculty of Medicine, University of Duisburg-Essen, Essen, Germany; Department of Gastroenterology, Hepatology and Infectious Diseases, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
[Ti] Título:Two separate mechanisms of enforced viral replication balance innate and adaptive immune activation.
[So] Source:J Autoimmun;67:82-89, 2016 Feb.
[Is] ISSN:1095-9157
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The induction of innate and adaptive immunity is essential for controlling viral infections. Limited or overwhelming innate immunity can negatively impair the adaptive immune response. Therefore, balancing innate immunity separately from activating the adaptive immune response would result in a better antiviral immune response. Recently, we demonstrated that Usp18-dependent replication of virus in secondary lymphatic organs contributes to activation of the innate and adaptive immune responses. Whether specific mechanisms can balance innate and adaptive immunity separately remains unknown. In this study, using lymphocytic choriomeningitis virus (LCMV) and replication-deficient single-cycle LCMV vectors, we found that viral replication of the initial inoculum is essential for activating virus-specific CD8(+) T cells. In contrast, extracellular distribution of virus along the splenic conduits is necessary for inducing systemic levels of type I interferon (IFN-I). Although enforced virus replication is driven primarily by Usp18, B cell-derived lymphotoxin beta contributes to the extracellular distribution of virus along the splenic conduits. Therefore, lymphotoxin beta regulates IFN-I induction independently of CD8(+) T-cell activity. We found that two separate mechanisms act together in the spleen to guarantee amplification of virus during infection, thereby balancing the activation of the innate and adaptive immune system.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Imunidade Inata
Replicação Viral/imunologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Interferon Tipo I/biossíntese
Linfonodos/imunologia
Linfonodos/metabolismo
Linfonodos/virologia
Ativação Linfocitária
Linfócitos/imunologia
Linfócitos/metabolismo
Coriomeningite Linfocítica/imunologia
Coriomeningite Linfocítica/virologia
Vírus da Coriomeningite Linfocítica/fisiologia
Linfotoxina-beta/metabolismo
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos
Camundongos Knockout
Baço/imunologia
Baço/metabolismo
Baço/virologia
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Ubiquitina Tiolesterase/genética
Ubiquitina Tiolesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interferon Type I); 0 (Lymphotoxin-beta); EC 3.4.19.- (Usp18 protein, mouse); EC 3.4.19.12 (Ubiquitin Thiolesterase)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170729
[Lr] Data última revisão:
170729
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151111
[St] Status:MEDLINE


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[PMID]:26403432
[Au] Autor:Weidemann A; Lovas A; Rauch A; Andreas N; von Maltzahn J; Riemann M; Weih F
[Ad] Endereço:Immunology, Leibniz Institute for Age Research - Fritz Lipmann Institute (FLI), Jena, Germany.
[Ti] Título:Classical and alternative NF-κB signaling cooperate in regulating adipocyte differentiation and function.
[So] Source:Int J Obes (Lond);40(3):452-9, 2016 Mar.
[Is] ISSN:1476-5497
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: Inflammation of adipose tissue (AT) is a central mediator of insulin resistance. However, the molecular mechanisms triggered by inflammatory cells are not fully understood. The aim of this study was to analyze the metabolic functions of lymphotoxin-ß-receptor (LTßR)-mediated alternative NF-κB signaling in adipocytes and to reveal its effects on body weight and insulin sensitivity in vivo. METHODS: RelB(FatKO) mice and littermate controls were treated with LTßR agonistic antibody (α-LTßR) or a LTßR antagonist (LTßR:Ig fusion protein) after feeding a high-fat diet or standard diet. Mice were analyzed by insulin tolerance and glucose tolerance tests prior to analysis by necropsy and qRT-PCR of abdominal white adipose tissue. 3T3-L1 preadipocytes and mouse embryonic fibroblasts were used for differentiation and expression analysis after treatment with α-LTßR and differentiation to adipocytes. The molecular mechanism was elucidated by chromatin immunoprecipitation and combinatorial treatment with α-LTßR and tumor necrosis factor (TNF). RESULTS: RelB(FatKO) mice showed improved insulin sensitivity despite increased adiposity and adipocyte hypertrophy. LTßR-induced activation of p52-RelB in 3T3-L1 cells attenuated adipogenesis and modulated adipocyte functions via transcriptional downregulation of peroxisome proliferator-activated receptor γ (PPARγ). This LTßR-mediated pathway was synergistically regulated via a TNF-induced increase in p100 and RelB expression and nuclear translocation. CONCLUSIONS: Our data describe an anti-adipogenic action of LTßR signaling and a novel synergism of alternative and classical NF-κB signaling in the regulation of adipocytes. In conclusion, this strong synergism between the two NF-κB pathways shows a method to inhibit adipocyte differentiation and to improve insulin sensitivity and can be a potential target to treat metabolic disorders more efficiently than with other known drugs.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Diferenciação Celular
Receptor beta de Linfotoxina/metabolismo
Linfotoxina-beta/farmacologia
NF-kappa B/metabolismo
Transdução de Sinais
Fator de Transcrição RelB/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipogenia
Animais
Modelos Animais de Doenças
Regulação da Expressão Gênica
Immunoblotting
Camundongos
Transcrição Genética
Fator de Necrose Tumoral alfa
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ltbr protein, mouse); 0 (Lymphotoxin beta Receptor); 0 (Lymphotoxin-beta); 0 (NF-kappa B); 0 (Relb protein, mouse); 0 (Tumor Necrosis Factor-alpha); 147337-75-5 (Transcription Factor RelB)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150926
[St] Status:MEDLINE
[do] DOI:10.1038/ijo.2015.198



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