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[PMID]:29374162
[Au] Autor:Broughton SE; Hercus TR; Nero TL; Kan WL; Barry EF; Dottore M; Cheung Tung Shing KS; Morton CJ; Dhagat U; Hardy MP; Wilson NJ; Downton MT; Schieber C; Hughes TP; Lopez AF; Parker MW
[Ad] Endereço:Australian Cancer Research Foundation Rational Drug Discovery Centre, St. Vincent's Institute of Medical Research, Fitzroy, VIC, 3065, Australia.
[Ti] Título:A dual role for the N-terminal domain of the IL-3 receptor in cell signalling.
[So] Source:Nat Commun;9(1):386, 2018 01 26.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The interleukin-3 (IL-3) receptor is a cell-surface heterodimer that links the haemopoietic, vascular and immune systems and is overexpressed in acute and chronic myeloid leukaemia progenitor cells. It belongs to the type I cytokine receptor family in which the α-subunits consist of two fibronectin III-like domains that bind cytokine, and a third, evolutionarily unrelated and topologically conserved, N-terminal domain (NTD) with unknown function. Here we show by crystallography that, while the NTD of IL3Rα is highly mobile in the presence of IL-3, it becomes surprisingly rigid in the presence of IL-3 K116W. Mutagenesis, biochemical and functional studies show that the NTD of IL3Rα regulates IL-3 binding and signalling and reveal an unexpected role in preventing spontaneous receptor dimerisation. Our work identifies a dual role for the NTD in this cytokine receptor family, protecting against inappropriate signalling and dynamically regulating cytokine receptor binding and function.
[Mh] Termos MeSH primário: Subunidade alfa de Receptor de Interleucina-3/química
Subunidade alfa de Receptor de Interleucina-3/metabolismo
Domínios Proteicos
Transdução de Sinais
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação/genética
Células COS
Linhagem Celular Tumoral
Cercopithecus aethiops
Cristalografia por Raios X
Células HEK293
Seres Humanos
Interleucina-3/química
Interleucina-3/genética
Interleucina-3/metabolismo
Subunidade alfa de Receptor de Interleucina-3/genética
Simulação de Dinâmica Molecular
Mutação
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL3RA protein, human); 0 (Interleukin-3); 0 (Interleukin-3 Receptor alpha Subunit)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180128
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02633-7


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[PMID]:28456746
[Au] Autor:Carretta M; de Boer B; Jaques J; Antonelli A; Horton SJ; Yuan H; de Bruijn JD; Groen RWJ; Vellenga E; Schuringa JJ
[Ad] Endereço:Department of Experimental Hematology, Cancer Research Centre Groningen, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
[Ti] Título:Genetically engineered mesenchymal stromal cells produce IL-3 and TPO to further improve human scaffold-based xenograft models.
[So] Source:Exp Hematol;51:36-46, 2017 07.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recently, NOD-SCID IL2Rγ (NSG) mice were implanted with human mesenchymal stromal cells (MSCs) in the presence of ceramic scaffolds or Matrigel to mimic the human bone marrow (BM) microenvironment. This approach allowed the engraftment of leukemic samples that failed to engraft in NSG mice without humanized niches and resulted in a better preservation of leukemic stem cell self-renewal properties. To further improve our humanized niche scaffold model, we genetically engineered human MSCs to secrete human interleukin-3 (IL-3) and thrombopoietin (TPO). In vitro, these IL-3- and TPO-producing MSCs were superior in expanding human cord blood (CB) CD34 hematopoietic stem/progenitor cells. MLL-AF9-transduced CB CD34 cells could be transformed efficiently along myeloid or lymphoid lineages on IL-3- and TPO-producing MSCs. In vivo, these genetically engineered MSCs maintained their ability to differentiate into bone, adipocytes, and other stromal components. Upon transplantation of MLL-AF9-transduced CB CD34 cells, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) developed in engineered scaffolds, in which a significantly higher percentage of myeloid clones was observed in the mouse compartments compared with previous models. Engraftment of primary AML, B-cell ALL, and biphenotypic acute leukemia (BAL) patient samples was also evaluated, and all patient samples could engraft efficiently; the myeloid compartment of the BAL samples was better preserved in the human cytokine scaffold model. In conclusion, we show that we can genetically engineer the ectopic human BM microenvironment in a humanized scaffold xenograft model. This approach will be useful for functional study of the importance of niche factors in normal and malignant human hematopoiesis.
[Mh] Termos MeSH primário: Diferenciação Celular
Engenharia Genética
Interleucina-3
Células Mesenquimais Estromais/metabolismo
Nicho de Células-Tronco
Trombopoetina
Tecidos Suporte/química
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Xenoenxertos
Seres Humanos
Interleucina-3/biossíntese
Interleucina-3/genética
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/metabolismo
Transplante de Células-Tronco Mesenquimais
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Transplante de Neoplasias
Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras B/metabolismo
Trombopoetina/biossíntese
Trombopoetina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL3 protein, human); 0 (Interleukin-3); 9014-42-0 (Thrombopoietin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29023488
[Au] Autor:Askmyr M; von Palffy S; Hansen N; Landberg N; Högberg C; Rissler M; Ågerstam H; Fioretos T
[Ad] Endereço:Department of Clinical Genetics, Lund University, Lund, Sweden.
[Ti] Título:Transgenic expression of human cytokines in immunodeficient mice does not facilitate myeloid expansion of BCR-ABL1 transduced human cord blood cells.
[So] Source:PLoS One;12(10):e0186035, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several attempts have been made to model chronic myeloid leukemia (CML) in a xenograft setting but expansion of human myeloid cells in immunodeficient mice has proven difficult to achieve. Lack of cross-reacting cytokines in the microenvironment of the mice has been proposed as a potential reason. In this study we have used NOD/SCID IL2-receptor gamma deficient mice expressing human SCF, IL-3 and GM-CSF (NSGS mice), that should be superior in supporting human, and particularly, myeloid cell engraftment, to expand BCR-ABL1 expressing human cells in order to model CML. NSGS mice transplanted with BCR-ABL1 expressing cells became anemic and had to be sacrificed due to illness, however, this was not accompanied by an expansion of human myeloid cells but rather we observed a massive expansion of human T-cells and macrophages/histiocytes. Importantly, control human cells without BCR-ABL1 expression elicited a similar reaction, although with a slight delay of disease induction, suggesting that while BCR-ABL1 contributes to the inflammatory reaction, the presence of normal human hematopoietic cells is detrimental for NSGS mice.
[Mh] Termos MeSH primário: Citocinas/genética
Sangue Fetal/citologia
Proteínas de Fusão bcr-abl/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Feminino
Sangue Fetal/transplante
Expressão Gênica
Fator Estimulador de Colônias de Granulócitos e Macrófagos/genética
Seres Humanos
Interleucina-3/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Masculino
Camundongos Endogâmicos NOD
Camundongos SCID
Camundongos Transgênicos
Transdução Genética
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCR-ABL1 fusion protein, human); 0 (Cytokines); 0 (IL3 protein, human); 0 (Interleukin-3); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[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:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186035


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[PMID]:28947270
[Au] Autor:Ito R; Nagai D; Igo N; Okuda Y; Sekine K; Ichimura E; Katano I; Mizushima T; Goto M; Ohnishi Y; Ito M; Okamoto K
[Ad] Endereço:Central Institute for Experimental Animals, 3-25-12 Tonomachi, Kawasaki-ku, Kawasaki, Kanagawa 210-0821, Japan.
[Ti] Título:A novel in vivo model for predicting myelotoxicity of chemotherapeutic agents using IL-3/GM-CSF transgenic humanized mice.
[So] Source:Toxicol Lett;281:152-157, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Evaluating myelotoxicity is essential for ensuring the safety of novel drugs before they are approved for clinical applications. Although in vivo prediction of the maximum tolerated doses (MTDs) of anticancer drugs is usually performed in rodents, the results are not always applicable to clinical treatment because drugs may have different effects in human and rodent cells. Previously, we generated a human IL-3 and GM-CSF transgenic humanized mouse (hu-IL-3/GM Tg), in which human granulocytes effectively differentiated after hematopoietic stem cell transplantation. In this study, we established a novel in vivo preclinical evaluation model for predicting human myelotoxicity of anticancer drugs using these hu-IL-3/GM Tg mice. The myelotoxicity was investigated by kinetic flow cytometry of human or murine granulocytes and by colony-forming unit granulocyte/macrophage (CFU-GM) assays. In both in vivo and in vitro analyses, topotecan was more myelotoxic to human than murine granulocytes. In contrast, oxaliplatin was more myelotoxic to murine granulocytes. The level of myelotoxicity of paclitaxel treatment was comparable between human and mouse cells. These results demonstrate that our humanized mouse model can simultaneously evaluate myelotoxicity against human and mouse cells in vivo, and provides an effective preclinical tool for predicting appropriate doses of anticancer agents for clinical treatment.
[Mh] Termos MeSH primário: Antineoplásicos Fitogênicos/toxicidade
Paclitaxel/toxicidade
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Ensaio de Unidades Formadoras de Colônias
Relação Dose-Resposta a Droga
Fator Estimulador de Colônias de Granulócitos e Macrófagos/genética
Granulócitos/efeitos dos fármacos
Células-Tronco Hematopoéticas/efeitos dos fármacos
Seres Humanos
Concentração Inibidora 50
Interleucina-3/genética
Camundongos
Camundongos Endogâmicos NOD
Camundongos Transgênicos
Testes de Toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Interleukin-3); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); P88XT4IS4D (Paclitaxel)
[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:170927
[St] Status:MEDLINE


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[PMID]:28821584
[Au] Autor:Kunnath-Velayudhan S; Goldberg MF; Saini NK; Johndrow CT; Ng TW; Johnson AJ; Xu J; Chan J; Jacobs WR; Porcelli SA
[Ad] Endereço:Department of Microbiology and Immunology, Albert Einstein College of Medicine, New York, NY 10461.
[Ti] Título:Transcriptome Analysis of Mycobacteria-Specific CD4 T Cells Identified by Activation-Induced Expression of CD154.
[So] Source:J Immunol;199(7):2596-2606, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Analysis of Ag-specific CD4 T cells in mycobacterial infections at the transcriptome level is informative but technically challenging. Although several methods exist for identifying Ag-specific T cells, including intracellular cytokine staining, cell surface cytokine-capture assays, and staining with peptide:MHC class II multimers, all of these have significant technical constraints that limit their usefulness. Measurement of activation-induced expression of CD154 has been reported to detect live Ag-specific CD4 T cells, but this approach remains underexplored and, to our knowledge, has not previously been applied in mycobacteria-infected animals. In this article, we show that CD154 expression identifies adoptively transferred or endogenous Ag-specific CD4 T cells induced by bacillus Calmette-Guérin vaccination. We confirmed that Ag-specific cytokine production was positively correlated with CD154 expression by CD4 T cells from bacillus Calmette-Guérin-vaccinated mice and show that high-quality microarrays can be performed from RNA isolated from CD154 cells purified by cell sorting. Analysis of microarray data demonstrated that the transcriptome of CD4 CD154 cells was distinct from that of CD154 cells and showed major enrichment of transcripts encoding multiple cytokines and pathways of cellular activation. One notable finding was the identification of a previously unrecognized subset of mycobacteria-specific CD4 T cells that is characterized by the production of IL-3. Our results support the use of CD154 expression as a practical and reliable method to isolate live Ag-specific CD4 T cells for transcriptomic analysis and potentially for a range of other studies in infected or previously immunized hosts.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Ligante de CD40/genética
Perfilação da Expressão Gênica/métodos
Ativação Linfocitária
Mycobacterium bovis/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Bactérias/imunologia
Ligante de CD40/análise
Ligante de CD40/deficiência
Citocinas/biossíntese
Citocinas/imunologia
Epitopos
Interleucina-3/biossíntese
Interleucina-3/imunologia
Camundongos
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Cytokines); 0 (Epitopes); 0 (Interleukin-3); 147205-72-9 (CD40 Ligand)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700654


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[PMID]:28811319
[Au] Autor:Carabelli J; Quattrocchi V; D'Antuono A; Zamorano P; Tribulatti MV; Campetella O
[Ad] Endereço:Laboratorio de Inmunología Molecular, Instituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomús, Universidad Nacional de San Martín, Consejo Nacional de Investigaciones Científicas y Técnicas, San Martín, Buenos Aires, Argentina.
[Ti] Título:Galectin-8 activates dendritic cells and stimulates antigen-specific immune response elicitation.
[So] Source:J Leukoc Biol;102(5):1237-1247, 2017 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Galectin-8 (Gal-8) is a mammalian ß-galactoside-binding lectin, endowed with proinflammatory properties. Given its capacity to enhance antigen-specific immune responses in vivo, we investigated whether Gal-8 was also able to promote APC activation to sustain T cell activation after priming. Both endogenous [dendritic cells (DCs)] and bone marrow-derived DCs (BMDCs) treated with exogenous Gal-8 exhibited a mature phenotype characterized by increased MHC class II (MHCII), CD80, and CD86 surface expression. Moreover, Gal-8-treated BMDCs (Gal-8-BMDCs) stimulated antigen-specific T cells more efficiently than immature BMDCs (iBMDCs). Proinflammatory cytokines IL-3, IL-2, IL-6, TNF, MCP-1, and MCP-5, as well as growth factor G-CSF, were augmented in Gal-8-BMDC conditioned media, with IL-6 as the most prominent. Remarkably, BMDCs from Gal-8-deficient mice ( BMDC) displayed reduced CD86 and IL-6 expression and an impaired ability to promote antigen-specific CD4 T cell activation. To test if Gal-8-induced activation correlates with the elicitation of an effective immune response, soluble Gal-8 was coadministrated with antigen during immunization of BALB/cJ mice in the experimental foot-and-mouth disease virus (FMDV) model. When a single dose of Gal-8 was added to the antigen formulation, an increased specific and neutralizing humoral response was developed, sufficient to enhance animal protection upon viral challenge. IL-6 and IFN-γ, as well as lymphoproliferative responses, were also incremented in Gal-8/antigen-immunized animals only at 48 h after immunization, suggesting that Gal-8 induces the elicitation of an inflammatory response at an early stage. Taking together, these findings argue in favor of the use of Gal-8 as an immune-stimulator molecule to enhance the adaptive immune response.
[Mh] Termos MeSH primário: Apresentação do Antígeno
Antígenos Virais/imunologia
Linfócitos T CD4-Positivos/imunologia
Células Dendríticas/imunologia
Febre Aftosa/imunologia
Galectinas/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Antígenos Virais/administração & dosagem
Antígenos Virais/genética
Linfócitos T CD4-Positivos/virologia
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Células Dendríticas/virologia
Febre Aftosa/genética
Febre Aftosa/prevenção & controle
Febre Aftosa/virologia
Vírus da Febre Aftosa/crescimento & desenvolvimento
Vírus da Febre Aftosa/imunologia
Galectinas/genética
Galectinas/farmacologia
Regulação da Expressão Gênica
Fator Estimulador de Colônias de Granulócitos/genética
Fator Estimulador de Colônias de Granulócitos/imunologia
Imunização
Interleucina-2/genética
Interleucina-2/imunologia
Interleucina-3/genética
Interleucina-3/imunologia
Interleucina-6/genética
Interleucina-6/imunologia
Ativação Linfocitária
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Proteínas Quimioatraentes de Monócitos/genética
Proteínas Quimioatraentes de Monócitos/imunologia
Transdução de Sinais
Fatores de Tempo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Viral); 0 (Ccl12 protein, mouse); 0 (Ccl2 protein, mouse); 0 (Chemokine CCL2); 0 (Galectins); 0 (Interleukin-2); 0 (Interleukin-3); 0 (Interleukin-6); 0 (Monocyte Chemoattractant Proteins); 0 (Tumor Necrosis Factor-alpha); 0 (galectin-8, mouse); 0 (interleukin-6, mouse); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3A0816-357RR


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[PMID]:28793897
[Au] Autor:Kim J; Lee YJ; Kim YA; Cho ES; Huh E; Bang OS; Kim NS
[Ad] Endereço:KM-Convergence Research Division, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon, 34054, Republic of Korea.
[Ti] Título:Aqueous extract of Phragmitis rhizoma ameliorates myelotoxicity of docetaxel in vitro and in vivo.
[So] Source:BMC Complement Altern Med;17(1):393, 2017 Aug 09.
[Is] ISSN:1472-6882
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A variety of anticancer chemotherapeutics induce adverse side effects including myelotoxicity. Dried roots of Phragmites communis Trinius, Phragmitis rhizoma, have been clinically used in traditional folk medicine to relieve various symptoms like fever. In this study, we evaluated the protective effect of the aqueous extract of Phragmitis rhizoma (EPR) against docetaxel-induced myelotoxicity in vitro and in vivo. METHODS: The in vitro myelo-protective effect of EPR was evaluated using the colony forming unit (CFU) assay with hematopoietic progenitor cells. The in vivo efficacy of EPR was evaluated in myelosuppressed C57BL/6 male mice which were induced by repeated intraperitoneal injections of 30 mg/kg docetaxel for 3 times. EPR was orally administered for 4 days to docetaxel-induced myelosuppressed C57BL/6 male mice which were induced by intraperitoneal injection of 30 mg/kg docetaxel for 3 times: Group 1 (vehicle control, n = 10), Group 2 (docetaxel plus vehicle, n = 10), Group 3 (docetaxel plus EPR 30 mg/kg, n = 10), Group 4 (docetaxel plus EPR 100 mg/kg, n = 10) and Group 5 (docetaxel plus EPR 300 mg/kg, n = 10). Whole blood counts were measured automatically, and immune organs were histologically examined. Expression of immunomodulatory cytokines was measured by quantitative real-time polymerase chain reaction or enzyme-linked immunosorbent assay. The toxicity of EPR itself was evaluated in normal human cell lines including IMR-90, foreskin fibroblast and human umbilical vein endothelial cells. The hepatotoxicity of EPR was predicted by multi-parametric assays involving cell viability, caspase 3/7 activity, GSH contents and LDH leakage using the HepaRG hepatic cell line. RESULTS: Co-treatment of EPR or its major component, p-hydroxycinnamic acid, increased the numbers of hematopoietic CFU counts in the docetaxel-induced in vitro myelotoxicity assay system. The in vitro protective effect of EPR against docetaxel toxicity was replicated in a myelosuppressed animal model: white blood cells, neutrophils, lymphocytes and red blood cells rebounded; bone marrow niche and structural integrity of the thymus were preserved; and the expression of immune-stimulating cytokines including IL3, IL6, SCF and GM-CSF was enhanced. Furthermore, EPR and p-hydroxycinnamic acid promoted the proliferation of primary splenocytes and thymocytes. In the toxicity assays, no remarkable signs related with toxicity were observed in all tested normal human cells and HepaRG. CONCLUSIONS: EPR has the potential to ameliorate docetaxel-mediated myelotoxicity in both in vitro and in vivo models. However, the identification of the responsible active components and the precise underlying myelo-protective mechanism of EPR need to be elucidated before novel drug development using EPR can precede.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Medula Óssea/efeitos dos fármacos
Ácidos Cumáricos/farmacologia
Células-Tronco Hematopoéticas/metabolismo
Extratos Vegetais/farmacologia
Poaceae
Taxoides/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Células Sanguíneas
Células da Medula Óssea
Fatores Estimuladores de Colônias/sangue
Ensaio de Imunoadsorção Enzimática
Fibroblastos
Hematopoese
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Interleucina-3/sangue
Interleucina-6/sangue
Camundongos Endogâmicos C57BL
Propionatos
Reação em Cadeia da Polimerase em Tempo Real
Rizoma
Baço/efeitos dos fármacos
Fator de Células-Tronco/sangue
Timo/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Colony-Stimulating Factors); 0 (Coumaric Acids); 0 (Interleukin-3); 0 (Interleukin-6); 0 (Plant Extracts); 0 (Propionates); 0 (Stem Cell Factor); 0 (Taxoids); 15H5577CQD (docetaxel); IBS9D1EU3J (trans-3-(4'-hydroxyphenyl)-2-propenoic acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1186/s12906-017-1890-1


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[PMID]:28753604
[Au] Autor:Demirel Ö; Balló O; Reddy PNG; Vakhrusheva O; Zhang J; Eichler A; Fernandes R; Badura S; Serve H; Brandts C
[Ad] Endereço:Department of Medicine, Hematology/Oncology, Goethe University, Frankfurt, Germany.
[Ti] Título:SOCS1 function in BCR-ABL mediated myeloproliferative disease is dependent on the cytokine environment.
[So] Source:PLoS One;12(7):e0180401, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment with tyrosine kinase inhibitors is the standard of care for Philadelphia chromosome positive leukemias. However the eradication of leukemia initiating cells remains a challenge. Circumstantial evidence suggests that the cytokine microenvironment may play a role in BCR-ABL mediated leukemogenesis and in imatinib resistance. Gene expression analyses of BCR-ABL positive ALL long-term cultured cells revealed strong reduction of SOCS mRNA expression after imatinib treatment, thereby demonstrating a strong inhibition of cytokine signaling. In this study we employed SOCS1-a strong inhibitor of cytokine signaling-as a tool to terminate external cytokine signals in BCR-ABL transformed cells in vitro and in vivo. In colony formation assays with primary bone marrow cells, expression of SOCS1 decreased colony numbers under pro-proliferative cytokines, while it conferred growth resistance to anti-proliferative cytokines. Importantly, co-expression of SOCS1 with BCR-ABL led to the development of a MPD phenotype with a prolonged disease latency compared to BCR-ABL alone in a murine bone marrow transplantation model. Interestingly, SOCS1 co-expression protected 20% of mice from MPD development. In summary, we conclude that under pro-proliferative cytokine stimulation at the onset of myeloproliferative diseases SOCS1 acts as a tumor suppressor, while under anti-proliferative conditions it exerts oncogenic function. Therefore SOCS1 can promote opposing functions depending on the cytokine environment.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Proteínas de Fusão bcr-abl/metabolismo
Transtornos Mieloproliferativos/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
[Mh] Termos MeSH secundário: Animais
Medula Óssea/metabolismo
Transplante de Medula Óssea
Linhagem Celular
Feminino
Proteínas de Fusão bcr-abl/genética
Interleucina-3/metabolismo
Camundongos
Transtornos Mieloproliferativos/genética
Fosforilação
Fator de Transcrição STAT5/metabolismo
Baço/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-3); 0 (STAT5 Transcription Factor); 0 (Socs1 protein, mouse); 0 (Suppressor of Cytokine Signaling 1 Protein); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180401


  9 / 6242 MEDLINE  
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[PMID]:28652400
[Au] Autor:Schroeder JT; Bieneman AP
[Ad] Endereço:Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224 schray@jhmi.edu.
[Ti] Título:Activation of Human Basophils by A549 Lung Epithelial Cells Reveals a Novel IgE-Dependent Response Independent of Allergen.
[So] Source:J Immunol;199(3):855-865, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Evidence for epithelial cell (EC)-derived cytokines (e.g., thymic stromal lymphopoietin [TSLP]) activating human basophils remains controversial. We therefore hypothesize that ECs can directly activate basophils via cell-to-cell interaction. Basophils in medium alone or with IL-3 ± anti-IgE were coincubated with TSLP, IL-33, or IL-25. Analogous experiments cocultured basophils (1-72 h) directly with EC lines. Supernatants were tested for mediators and cytokines. Abs targeting receptors were tested for neutralizing effects. Lactic acid (pH 3.9) treatment combined with passive sensitization tested the role of IgE. Overall, IL-33 augmented IL-13 secretion from basophils cotreated with IL-3, with minimal effects on histamine and IL-4. Conversely, basophils (but not mast cells) released histamine and marked levels of IL-4/IL-13 (10-fold) when cocultured with A549 EC and IL-3, without exogenous allergen or IgE cross-linking stimuli. The inability to detect IL-33 or TSLP, or to neutralize their activity, suggested a unique mode of basophil activation by A549 EC. Half-maximal rates for histamine (4 h) and IL-4 (5 h) secretion were slower than observed with standard IgE-dependent activation. Ig stripping combined with passive sensitization ± omalizumab showed a dependency for basophil-bound IgE, substantiated by a requirement for cell-to-cell contact, aggregation, and FcεRI-dependent signaling. A yet unidentified IgE-binding lectin associated with A549 EC is implicated after discovering that LacNAc suppressed basophil activation in cocultures. These findings point to a lectin-dependent activation of basophil requiring IgE but independent of allergen or secreted cytokine. Pending further investigation, we predict this unique mode of activation is linked to inflammatory conditions whereby IgE-dependent activation of basophils occurs despite the absence of any known allergen.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Basófilos/imunologia
Células Epiteliais/imunologia
Imunoglobulina E/imunologia
[Mh] Termos MeSH secundário: Células A549
Anticorpos Anti-Idiotípicos/farmacologia
Basófilos/efeitos dos fármacos
Basófilos/metabolismo
Comunicação Celular
Técnicas de Cocultura
Citocinas/farmacologia
Citocinas/secreção
Células Epiteliais/metabolismo
Liberação de Histamina
Seres Humanos
Imunoglobulina E/metabolismo
Interleucina-13/imunologia
Interleucina-13/secreção
Interleucina-17/farmacologia
Interleucina-3/imunologia
Interleucina-3/farmacologia
Interleucina-33/farmacologia
Interleucina-4/imunologia
Interleucina-4/secreção
Ácido Láctico/farmacologia
Lectinas/metabolismo
Mastócitos/metabolismo
Omalizumab/farmacologia
Receptores de IgE/imunologia
Receptores de IgE/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Antibodies, Anti-Idiotypic); 0 (Cytokines); 0 (FcepsilonRI alpha-chain, human); 0 (IL25 protein, human); 0 (IL3 protein, human); 0 (IL33 protein, human); 0 (Interleukin-13); 0 (Interleukin-17); 0 (Interleukin-3); 0 (Interleukin-33); 0 (Lectins); 0 (Receptors, IgE); 0 (anti-IgE antibodies); 0 (interleukin-13, human); 0 (thymic stromal lymphopoietin); 207137-56-2 (Interleukin-4); 2P471X1Z11 (Omalizumab); 33X04XA5AT (Lactic Acid); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700055


  10 / 6242 MEDLINE  
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[PMID]:28629733
[Au] Autor:Yin Y; Bai Y; Olivera A; Desai A; Metcalfe DD
[Ad] Endereço:Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases,National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: yiny@niaid.nih.gov.
[Ti] Título:An optimized protocol for the generation and functional analysis of human mast cells from CD34 enriched cell populations.
[So] Source:J Immunol Methods;448:105-111, 2017 Sep.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The culture of mast cells from human tissues such a cord blood, peripheral blood or bone marrow aspirates has advanced our understanding of human mast cells (huMC) degranulation, mediator production and response to pharmacologic agents. However, existing methods for huMC culture tend to be laborious and expensive. Combining technical approaches from several of these protocols, we designed a simplified and more cost effective approach to the culture of mast cells from human cell populations including peripheral blood and cryopreserved cells from lymphocytapheresis. On average, we reduced by 30-50 fold the amount of culture media compared to our previously reported method, while the total MC number generated by this method (2.46±0.63×10 vs. 2.4±0.28×10 , respectively, from 1.0×10 lymphocytapheresis or peripheral blood mononuclear blood cells [PBMCs]) was similar to our previous method (2.36±0.70×10 ), resulting in significant budgetary savings. In addition, we compared the yield of huMCs with or without IL-3 added to early cultures in the presence of stem cell factor (SCF) and interlukin-6 (IL-6) and found that the total MC number generated, while higher with IL-3 in the culture, did not reach statistical significance, suggesting that IL-3, often recommended in the culture of huMCs, is not absolutely required. We then performed a functional analysis by flow cytometry using standard methods and which maximized the data we could obtain from cultured cells. We believe these approaches will allow more laboratories to culture and examine huMC behavior going forward.
[Mh] Termos MeSH primário: Antígenos CD34/metabolismo
Separação Celular/métodos
Leucaférese
Mastócitos/metabolismo
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Antígenos CD34/imunologia
Biomarcadores/metabolismo
Orçamentos
Degranulação Celular
Diferenciação Celular
Linhagem da Célula
Proliferação Celular
Separação Celular/economia
Forma Celular
Células Cultivadas
Redução de Custos
Análise Custo-Benefício
Criopreservação
Meios de Cultura/metabolismo
Citometria de Fluxo
Seres Humanos
Interleucina-3/farmacologia
Interleucina-6/farmacologia
Leucaférese/economia
Mastócitos/efeitos dos fármacos
Mastócitos/imunologia
Fenótipo
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptores de IgE/metabolismo
Fator de Células-Tronco/farmacologia
Células-Tronco/efeitos dos fármacos
Células-Tronco/imunologia
Fatores de Tempo
Fluxo de Trabalho
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Biomarkers); 0 (Culture Media); 0 (IL3 protein, human); 0 (IL6 protein, human); 0 (Interleukin-3); 0 (Interleukin-6); 0 (Receptors, IgE); 0 (Stem Cell Factor); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE



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