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Pesquisa : D12.776.543.750.705.852.420.500 [Categoria DeCS]
Referências encontradas : 109 [refinar]
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  1 / 109 MEDLINE  
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[PMID]:28450306
[Au] Autor:Xiao M; Wang Y; Tao C; Wang Z; Yang J; Chen Z; Zou Z; Li M; Liu A; Jia C; Huang B; Yan B; Lai P; Ding C; Cai D; Xiao G; Jiang Y; Bai X
[Ad] Endereço:State Key Laboratory of Organ Failure Research, Department of Cell Biology, School of Basic Medical Sciences and.
[Ti] Título:Osteoblasts support megakaryopoiesis through production of interleukin-9.
[So] Source:Blood;129(24):3196-3209, 2017 06 15.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Severe thrombocytopenia is a significant challenge in patients undergoing myelosuppressive chemotherapy for malignancies. Understanding the biology of platelet-producing megakaryocytes development in the bone marrow microenvironment may facilitate the development of novel therapies to stimulate platelet production and prevent thrombocytopenia. We report here that osteoblasts supported megakaryopoiesis by secreting interleukin-9 (IL-9), which stimulated IL-9 receptor (IL-9R)/Stat3 signaling in promoting megakaryopoiesis. IL-9 production in osteoblasts was negatively regulated by the mechanistic target of rapamycin complex 1 (mTORC1) signaling in a NF-κB-dependent manner. Constitutive activation of mTORC1 inhibited IL-9 production in osteoblasts and suppressed megakaryocytic cells expansion, whereas mTORC1 inactivation increased IL-9 production and enhanced megakaryocyte and platelet numbers in mice. In mouse models, we showed that IL-9 administration stimulated megakaryopoiesis, whereas neutralizing endogenous IL-9 or IL-9R depletion inhibited the process. Importantly, we found that low doses of IL-9 efficiently prevented chemotherapy-induced thrombocytopenia (CIT) and accelerated platelet recovery after CIT. These data indicate that IL-9 is an essential regulator of megakaryopoiesis and a promising therapeutic agent for treatment of thrombocytopenia such as CIT.
[Mh] Termos MeSH primário: Interleucina-9/metabolismo
Megacariócitos/metabolismo
Osteoblastos/metabolismo
Transdução de Sinais/fisiologia
Trombopoese/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Alvo Mecanístico do Complexo 1 de Rapamicina
Megacariócitos/citologia
Camundongos
Complexos Multiproteicos/metabolismo
Osteoblastos/citologia
Células RAW 264.7
Receptores de Interleucina-9/metabolismo
Fator de Transcrição STAT3/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL9 protein, human); 0 (IL9R protein, human); 0 (Il9r protein, mouse); 0 (Interleukin-9); 0 (Multiprotein Complexes); 0 (Receptors, Interleukin-9); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Stat3 protein, mouse); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-11-749838


  2 / 109 MEDLINE  
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[PMID]:28681919
[Au] Autor:Guggino G; Lo Pizzo M; Di Liberto D; Rizzo A; Cipriani P; Ruscitti P; Candore G; Gambino CM; Sireci G; Dieli F; Giacomelli R; Triolo G; Ciccia F
[Ad] Endereço:Dipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, Università di Palermo, Palermo, Italy.
[Ti] Título:Interleukin-9 over-expression and T helper 9 polarization in systemic sclerosis patients.
[So] Source:Clin Exp Immunol;190(2):208-216, 2017 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:T helper 9 (Th9) cells and interleukin (IL)-9 are involved in the pathogenesis of several autoimmune diseases. The exact role of IL-9 and Th9 cells in patients with systemic sclerosis (SSc) have not yet been studied adequately. IL-9, IL-9R, transcription factor PU.1 (PU.1), IL-4, thymic stromal lymphopoietin (TSLP) and transforming growth factor (TGF)-ß expression were assessed in skin and kidney biopsies of SSc patients and healthy controls (HC) by immunohistochemistry (IHC). The cellular source of IL-9 was also analysed by confocal microscopy analysis. Peripheral IL-9-producing cells were also studied by flow cytometry. The functional relevance of IL-9 increased expression in SSc was also investigated. Our results demonstrated a strong expression of IL-9, IL-9R, IL-4, TSLP and TGF-ß in skin tissues of patients with both limited and diffuse SSc. IL-9 expression was observed mainly in the context of skin infiltrating mononuclear cells and keratinizing squamous epithelium. IL-9 over-expression was also observed in renal biopsies of patients with SSc. IL-9 producing cells in the skin were identified as Th9 cells. Similarly, Th9 cells were expanded and were the major source of IL-9 among SSc peripheral blood mononuclear cells (PBMC), their percentage being correlated directly with the modified Rodnan skin score. Infiltrating mononuclear cells, mast cells and neutrophils expressed IL-9R. In in-vitro studies stimulation with rIL-9 significantly induced NET (neutrophil extracellular traps) release by dying cells (NETosis) in neutrophils, expansion of mast cells and increase of anti-systemic scleroderma 70 (Scl70) production by B cells. Our findings suggest that Th9 cells and IL-9 could be implicated in the pathogenesis of SSc.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Interleucina-9/metabolismo
Escleroderma Sistêmico/imunologia
[Mh] Termos MeSH secundário: Adulto
Autoanticorpos/sangue
Linfócitos B/efeitos dos fármacos
Linfócitos T CD4-Positivos/classificação
Linfócitos T CD4-Positivos/metabolismo
Diferenciação Celular
Citocinas/genética
Citocinas/metabolismo
Armadilhas Extracelulares/metabolismo
Feminino
Seres Humanos
Interleucina-4/genética
Interleucina-4/metabolismo
Interleucina-9/sangue
Interleucina-9/genética
Interleucina-9/imunologia
Masculino
Mastócitos/imunologia
Mastócitos/metabolismo
Meia-Idade
Neutrófilos/imunologia
Neutrófilos/metabolismo
Proteínas Proto-Oncogênicas/genética
Proteínas Proto-Oncogênicas/metabolismo
Receptores de Interleucina-9/genética
Receptores de Interleucina-9/metabolismo
Escleroderma Sistêmico/fisiopatologia
Pele/imunologia
Pele/metabolismo
Pele/patologia
Transativadores/genética
Transativadores/metabolismo
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Cytokines); 0 (IL4 protein, human); 0 (IL9 protein, human); 0 (Interleukin-9); 0 (Proto-Oncogene Proteins); 0 (Receptors, Interleukin-9); 0 (Trans-Activators); 0 (Transforming Growth Factor beta); 0 (proto-oncogene protein Spi-1); 0 (thymic stromal lymphopoietin); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13009


  3 / 109 MEDLINE  
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[PMID]:27896635
[Au] Autor:Schmitt E; Bopp T
[Ad] Endereço:Institute for Immunology, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, Bd. 708, 55131, Mainz, Germany. eschmitt@uni-mainz.de.
[Ti] Título:Discovery and initial characterization of Th9 cells: the early years.
[So] Source:Semin Immunopathol;39(1):5-10, 2017 Jan.
[Is] ISSN:1863-2300
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The launch of the Th1/Th2 concept represented a decisive breakthrough concerning our understanding of how very diverse immune reactions can be regulated by functionally different T helper subpopulations via the secretion of different panels of cytokines. In this context, IL-9 was identified to be produced by T helper cell lines in addition to Th2 cytokines IL-4 and IL-5. Detailed analyses revealed that IL-9 production of mouse CD4 T helper cells was dependent on a combination of IL-2, IL-4, and TGF-ß. Roughly a decade later, it was found that TGF-ß can also induce the development of CD4 Treg cells. This finding engendered a series of studies on the central role of TGF-ß for cytokine-mediated T helper cell differentiation which elucidated that IL-4 curbed the Treg cell-promoting effect of TGF-ß while TGF-ß impaired the Th2-promoting capacity of IL-4. Instead, TGF-ß in combination with IL-4 induced the development of CD4 T helper cells that preferentially produced IL-9 and that were different from Th2 cells which originally were thought to be the main source of IL-9. In addition, adoptive transfer of such IL-9-producing CD4 T helper cells was shown to cause the development of colitis and peripheral neuritis. Hence, the unique cytokine expression pattern in combination with the inflammatory in vivo phenotype led to the designation of Th9 cells as a new CD4 T helper subpopulation.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Auxiliares-Indutores/metabolismo
[Mh] Termos MeSH secundário: Animais
Clonagem Molecular
Citocinas/metabolismo
Regulação da Expressão Gênica
História do Século XX
Seres Humanos
Interleucina-9/genética
Camundongos
Receptores de Interleucina-9/genética
Pesquisa/história
Subpopulações de Linfócitos T/citologia
Linfócitos T Auxiliares-Indutores/citologia
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-9); 0 (Receptors, Interleukin-9)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161130
[St] Status:MEDLINE
[do] DOI:10.1007/s00281-016-0610-0


  4 / 109 MEDLINE  
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[PMID]:27858144
[Au] Autor:Koch S; Sopel N; Finotto S
[Ad] Endereço:Department of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, 91052, Erlangen, Germany.
[Ti] Título:Th9 and other IL-9-producing cells in allergic asthma.
[So] Source:Semin Immunopathol;39(1):55-68, 2017 Jan.
[Is] ISSN:1863-2300
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Allergic asthma is a worldwide increasing chronic disease of the airways which affects more than 300 million people. It is associated with increased IgE, mast cell activation, airway hyperresponsiveness (AHR), mucus overproduction and remodeling of the airways. Previously, this pathological trait has been associated with T helper type 2 (Th2) cells. Recently, different CD4 T cell subsets (Th17, Th9) as well as cells of innate immunity, like mast cells and innate lymphoid cells type 2 (ILC2s), which are all capable of producing the rediscovered cytokine IL-9, are known to contribute to this disease. Regarding Th9 cells, it is known that naïve T cells develop into IL-9-producing cells in the presence of interleukin-4 (IL-4) and transforming growth factor beta (TGFß). Downstream of IL-4, several transcription factors like signal transducer and activator of transcription 6 (STAT6), interferon regulatory factor 4 (IRF4), GATA binding protein 3 (GATA3), basic leucine zipper transcription factor, ATF-like (BATF) and nuclear factor of activated T cells (NFAT) are activated. Additionally, the transcription factor PU.1, which is downstream of TGFß signaling, also seems to be crucial in the development of Th9 cells. IL-9 is a pleiotropic cytokine that influences various distinct functions of different target cells such as T cells, B cells, mast cells and airway epithelial cells by activating STAT1, STAT3 and STAT5. Because of its pleiotropic functions, IL-9 has been demonstrated to be involved in several diseases, such as cancer, autoimmunity and other pathogen-mediated immune-regulated diseases. In this review, we focus on the role of Th9 and IL-9-producing cells in allergic asthma.
[Mh] Termos MeSH primário: Asma/imunologia
Asma/metabolismo
Interleucina-9/metabolismo
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Auxiliares-Indutores/metabolismo
[Mh] Termos MeSH secundário: Animais
Asma/genética
Asma/patologia
Citocinas/metabolismo
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Sistema Imunitário/citologia
Sistema Imunitário/imunologia
Sistema Imunitário/metabolismo
Imunidade Inata/imunologia
Interleucina-9/genética
Mastócitos/imunologia
Mastócitos/metabolismo
Mastócitos/patologia
Receptores de Interleucina-9/metabolismo
Transdução de Sinais
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-9); 0 (Receptors, Interleukin-9); 0 (Transcription Factors)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161119
[St] Status:MEDLINE
[do] DOI:10.1007/s00281-016-0601-1


  5 / 109 MEDLINE  
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[PMID]:27543964
[Au] Autor:Guggino G; Ciccia F; Di Liberto D; Lo Pizzo M; Ruscitti P; Cipriani P; Ferrante A; Sireci G; Dieli F; Fourniè JJ; Giacomelli R; Triolo G
[Ad] Endereço:Dipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, Università degli Studi di Palermo.
[Ti] Título:Interleukin (IL)-9/IL-9R axis drives γδ T cells activation in psoriatic arthritis patients.
[So] Source:Clin Exp Immunol;186(3):277-283, 2016 Dec.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cytokines such as tumour necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, IL-23 and, more recently, IL-9, have been implicated in the initiation/maintenance of inflammation in psoriasis and psoriatic arthritis (PsA). In the present study we aimed to characterize the role of γδ T cells in peripheral blood and synovial fluid of PsA patients and to investigate their response to in-vitro stimulation with antigen or cytokines (IL-9 and IL-23). γδ T cells isolated from peripheral blood mononuclear cells and synovial fluid were analysed by flow cytometry to evaluate the phenotype and cytokine production. IL-23R and IL-9R gene expression were also evaluated by reverse transcription-polymerase chain reaction (RT-PCR). Peripheral blood mononuclear cells (PBMC), sorted γδ T cells and γδ cell lines were also stimulated in vitro with isopentenyl pyrophosphate (IPP), recombinant IL-9 or recombinant IL-23. Our results show an expansion of γδ T cells with a predominant effector memory phenotype in peripheral blood and synovium of untreated PsA patients, which reverses significantly after treatment with anti-TNF-α or anti-IL-12/IL-23R monoclonal antibodies (mAbs). Moreover, in PsA patients γδ T cells activation is driven prevalently by IL-9/IL-9R interaction, and not only by IL-23/IL-23R. Together these findings indicate γδ T cells and IL-9 as new players in the pathogenesis of PsA.
[Mh] Termos MeSH primário: Artrite Psoriásica/imunologia
Artrite Psoriásica/metabolismo
Interleucina-9/metabolismo
Ativação Linfocitária/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Receptores de Interleucina-9/metabolismo
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Artrite Psoriásica/diagnóstico
Artrite Psoriásica/tratamento farmacológico
Biomarcadores
Feminino
Seres Humanos
Imunofenotipagem
Masculino
Meia-Idade
Fenótipo
Índice de Gravidade de Doença
Líquido Sinovial/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-9); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin-9)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160821
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12853


  6 / 109 MEDLINE  
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[PMID]:27094152
[Au] Autor:Parrot T; Allard M; Oger R; Benlalam H; Raingeard de la Blétière D; Coutolleau A; Preisser L; Desfrançois J; Khammari A; Dréno B; Labarrière N; Delneste Y; Guardiola P; Gervois N
[Ad] Endereço:INSERM, U892, Nantes, France.
[Ti] Título:IL-9 promotes the survival and function of human melanoma-infiltrating CD4(+) CD8(+) double-positive T cells.
[So] Source:Eur J Immunol;46(7):1770-82, 2016 Jul.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:We previously demonstrated an accumulation of tumor-reactive CD4(+) CD8(+) double positive (DP) T cells within melanoma-infiltrating lymphocytes, supporting their role in the regulation of anti-tumor immune responses. Similarly to their CD8(+) counterparts, intra-tumor DP T cells are MHC class-I restricted but differed by a limited lytic activity against autologous melanoma cells. Based on these observations and to further characterize DP T cells, both populations were compared at the transcriptional level. Our results revealed the overexpression of the IL-9 receptor (IL-9R) by DP T cells and prompted us to investigate the impact of IL-9 on their biology. We show that IL-9 favors DP T-cell survival by protecting them from apoptosis and by promoting their proliferation. In addition, IL-9 enhances their ability to produce cytokines and increased their levels of granzyme B/perforin as well as degranulation capacity, leading to a strengthened cytotoxic activity against melanoma cells. Taken together, the IL-9R(high) DP T-cell population could be a new preferential target for IL-9, which could take part in their retention within the melanoma infiltrate while also favoring their anti-tumor activity. More generally, our results extend the pleiotropic effects of IL-9 to IL-9R-expressing intra-tumor T cells, which could further potentiate anti-tumor immune responses.
[Mh] Termos MeSH primário: Interleucina-9/imunologia
Linfócitos do Interstício Tumoral/imunologia
Linfócitos do Interstício Tumoral/metabolismo
Melanoma/imunologia
Melanoma/metabolismo
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/metabolismo
Sobrevivência Celular/imunologia
Células Cultivadas
Citocinas/metabolismo
Citotoxicidade Imunológica/efeitos dos fármacos
Expressão Gênica
Seres Humanos
Interleucina-9/farmacologia
Ativação Linfocitária/efeitos dos fármacos
Ativação Linfocitária/imunologia
Linfócitos do Interstício Tumoral/efeitos dos fármacos
Melanoma/genética
Melanoma/patologia
Receptores de Interleucina-9/genética
Receptores de Interleucina-9/metabolismo
Subpopulações de Linfócitos T/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-9); 0 (Receptors, Interleukin-9)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160421
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201546061


  7 / 109 MEDLINE  
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[PMID]:26216406
[Au] Autor:Ding X; Cao F; Cui L; Ciric B; Zhang GX; Rostami A
[Ad] Endereço:Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA; Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest of China, Colle
[Ti] Título:IL-9 signaling affects central nervous system resident cells during inflammatory stimuli.
[So] Source:Exp Mol Pathol;99(3):570-4, 2015 Dec.
[Is] ISSN:1096-0945
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL) 9, a dominant cytokine in Th9 cells, has been proven to play a pathogenic role in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by augmenting T cell activation and differentiation; however, whether IL-9 signaling affects central nervous system (CNS)-resident cells during CNS autoimmunity remains unknown. In the present study, we found that the IL-9 receptor (IL-9R) was highly expressed in astrocytes, oligodendrocyte progenitor cells (OPCs), oligodendrocytes and microglia cells, and that its expression was significantly upregulated in brain and spinal cord during EAE. In addition, IL-9 increased chemokine expression, including CXCL9, CCL20 and MMP3, in primary astrocytes. Although IL-9 had no effect on the proliferation of microglia cells, it decreased OPC proliferation and differentiation when in combination with other pro-inflammatory cytokines, but not with IFN-γ. IL-9 plus IFN-γ promoted OPC proliferation and differentiation. These findings indicate that CNS-restricted IL-9 signaling may be involved in the pathogenesis of MS/EAE, thus providing a potential therapeutic target for future MS/EAE treatment through disruption of CNS cell-specific IL-9 signaling.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/imunologia
Interleucina-9/imunologia
Neuroglia/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Animais
Astrócitos/imunologia
Autoimunidade/imunologia
Feminino
Imuno-Histoquímica
Inflamação/imunologia
Ativação Linfocitária/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Microglia/imunologia
Oligodendroglia/imunologia
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Interleucina-9/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Il9r protein, mouse); 0 (Interleukin-9); 0 (Receptors, Interleukin-9)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:151215
[Lr] Data última revisão:
151215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150729
[St] Status:MEDLINE


  8 / 109 MEDLINE  
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[PMID]:26082242
[Au] Autor:Li HJ; Sun QM; Liu LZ; Zhang J; Huang J; Wang CH; Ding R; Song K; Tong Z
[Ad] Endereço:Department of Hepatobiliary Surgery, The First People's Hospital of Hefei, Anhui 230000, P.R. China.
[Ti] Título:High expression of IL-9R promotes the progression of human hepatocellular carcinoma and indicates a poor clinical outcome.
[So] Source:Oncol Rep;34(2):795-802, 2015 Aug.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Interleukin-9 receptor (IL-9R) overexpression has a pivotal role in human hematological malignancies. However, the expression of IL-9R and its biological role in human solid tumors remains elusive. In the present study, western blot analysis and RT-qPCR were used to determine the expression of IL-9R in hepatocellular carcinoma (HCC) cell lines and tumor tissues. Proliferation, cell cycle, apoptosis and Transwell assays were used to examine the biological role of IL-9R in HCC cells. The results showed that IL-9R and its ligand IL-9 were constitutively expressed in HCC cells and tissues. Moreover, the expression levels of IL-9R and IL-9 were significantly higher in tumor tissues compared to the peritumor liver tissues. Functional experiments suggested that IL-9R significantly promoted HCC cell proliferation, invasion and inhibited apoptosis, possibly by acting through the IL-9/IL-9R axis. After silencing IL-9R, the expression of VEGF, p-p38, p-STAT3 and MMP9, markedly decreased suggesting the potential involvement of these molecules in IL-9R activity. Immunohistochemistry­based survival analysis revealed that a differential expression of IL-9R in HCC tissue was a significant and independent prognostic factor for survival [HR, 1.66; 95% confidence interval (CI), 1.17-2.36; P=0.005] and recurrence [HR, 1.50; 95%CI, 1.04­2.17; P=0.03]. In addition, a high IL-9R expression positively and significantly correlated with larger (P=0.012) and advanced tumor stage (P=0.018). The findings indicated that IL-9R was constitutively expressed and exerted a tumor-promoting effect in HCC, whose expression level may be a useful biomarker of tumor invasiveness and patient clinical outcome.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Carcinoma Hepatocelular/genética
Neoplasias Hepáticas/genética
Recidiva Local de Neoplasia/genética
Receptores de Interleucina-9/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Apoptose/genética
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Proliferação Celular/genética
Feminino
Seres Humanos
Neoplasias Hepáticas/patologia
Masculino
Meia-Idade
Invasividade Neoplásica/genética
Proteínas de Neoplasias/biossíntese
Recidiva Local de Neoplasia/patologia
Prognóstico
Receptores de Interleucina-9/biossíntese
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Neoplasm Proteins); 0 (Receptors, Interleukin-9)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150703
[Lr] Data última revisão:
150703
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150618
[St] Status:MEDLINE
[do] DOI:10.3892/or.2015.4060


  9 / 109 MEDLINE  
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[PMID]:25840641
[Au] Autor:Hong CH; Chang KL; Wang HJ; Yu HS; Lee CH
[Ad] Endereço:Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Dermatology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; Department of Dermatology, National Yang-Ming University College of Medicine, Taipei, Taiwan.
[Ti] Título:IL-9 induces IL-8 production via STIM1 activation and ERK phosphorylation in epidermal keratinocytes: A plausible mechanism of IL-9R in atopic dermatitis.
[So] Source:J Dermatol Sci;78(3):206-14, 2015 Jun.
[Is] ISSN:1873-569X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: IL-9 and its receptor play important roles in the pathogenesis of asthma. Its role in atopic dermatitis (AD) was examined in just a few studies, including nucleotide polymorphisms, increased transcriptional levels of IL-9 and IL-9R in diseased skin, and an association of blood IL-9 levels with clinical severity. OBJECTIVE: Little was known about the pathophysiological regulation of IL-9/IL-9R in AD skin. We asked whether IL-9R was expressed in epidermal keratinocytes; if so, what the functional outcome, cytokine production, and signaling pathway of IL-9/IL-9R in keratinocytes are. METHODS: We measured and compared the expression of IL-9R in skin from AD patients and controls by immunofluorescence. We also performed in vitro studies on the IL-9-treated primary keratinocytes, including flow cytometry for IL-9R expressions, Western blotting for mTOR, S6K, ERK, p38, and STAT3 activations, ELISA for cytokine levels, and immunofluorescence for STIM1. RESULTS: We found that IL-9R was indeed expressed in keratinocytes but not in fibroblasts. Its expression in keratinocytes was enhanced by IL-4 but not by TGF-beta1. IL-9 induced a moderate production of IL-8 but not CXCL16, CCL22, TSLP, nor IL-33. IL-9 induced formation of STIM1-puncta. IL-9 induced ERK phosphorylation both dose- and time-dependently, but not mTOR, S6K, p38, or STAT3. Pretreatment with U0126 (ERK inhibitor) but not rapamycin (mTOR inhibitor) abrogated the IL-9-mediated IL-8 production. Blockage of STIM1 with BTP2 or SKF96265 abrogated ERK phosphorylation and IL-8 production induced by IL-9. CONCLUSION: This study represents the first to show the regulation of the IL-9-STIM1-ERK-IL-8 axis in keratinocyte, and how the axis might play an important role in the pathophysiology of AD.
[Mh] Termos MeSH primário: Dermatite Atópica/etiologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Interleucina-8/biossíntese
Interleucina-9/farmacologia
Queratinócitos/metabolismo
Proteínas de Membrana/fisiologia
Proteínas de Neoplasias/fisiologia
Receptores de Interleucina-9/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Epiderme/citologia
Feminino
Seres Humanos
Interleucina-4/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Fosforilação
Molécula 1 de Interação Estromal
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL9R protein, human); 0 (Interleukin-8); 0 (Interleukin-9); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (Receptors, Interleukin-9); 0 (STIM1 protein, human); 0 (Stromal Interaction Molecule 1); 207137-56-2 (Interleukin-4); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150405
[St] Status:MEDLINE


  10 / 109 MEDLINE  
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[PMID]:25784693
[Au] Autor:Zhang W; Tang T; Nie D; Wen S; Jia C; Zhu Z; Xia N; Nie S; Zhou S; Jiao J; Dong W; Lv B; Xu T; Sun B; Lu Y; Li Y; Cheng L; Liao Y; Cheng X
[Ad] Endereço:Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430022, China Key Laboratory of Biological Targeted Therapy of the Ministry of Education, Wuhan 430022, China.
[Ti] Título:IL-9 aggravates the development of atherosclerosis in ApoE-/- mice.
[So] Source:Cardiovasc Res;106(3):453-64, 2015 Jun 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: Recently, interleukin (IL)-9 was found to be involved in the pathogenesis of many inflammatory diseases. Here, we tested whether IL-9 was related to atherosclerosis and investigated the underlying mechanisms. METHODS AND RESULTS: IL-9R was expressed in mouse aortic endothelial cells (MAECs) and aortic tissues, and IL-9 levels were elevated in plasma and aortic arches in Apolipoprotein E-deficient (ApoE-/-) mice. ApoE-/- mice fed a western diet for 10 weeks were administered recombinant mouse IL-9 (rIL-9) or anti-IL-9 neutralizing monoclonal antibody (mAb). Mice treated with rIL-9 developed markedly larger plaques in both the aorta and aortic root. Immunohistochemical studies demonstrated increases in both vascular endothelial adhesion molecule-1 (VCAM-1) expression and the infiltration of inflammatory cells, including T cells and macrophages, in plaques. However, treatment with the anti-IL-9 mAb caused the opposite effect. The administration of rIL-9 did not affect the splenic T cell or peripheral monocyte subsets. Meanwhile, IL-9 induced VCAM-1 expression in MAECs mainly via a STAT3-dependent pathway, consequently increasing monocyte-endothelial adhesion. Moreover, treatment with anti-VCAM-1 mAb partially abrogated the IL-9-induced increase in plaque area. In addition, CD4(+)IL-9(+) T cells and IL-9 were increased in patients with acute coronary syndrome, and the levels of IL-9 in culture supernatants and soluble VCAM-1 (sVCAM-1) in plasma were significantly positively correlated in the enrolled patients. CONCLUSION: Our results demonstrated that IL-9 exerted pro-atherosclerotic effects in ApoE-/- mice at least partially by inducing VCAM-1 expression, which mediated inflammatory cell infiltration into atherosclerotic lesions.
[Mh] Termos MeSH primário: Aorta Torácica/metabolismo
Doenças da Aorta/metabolismo
Apolipoproteínas E/deficiência
Aterosclerose/metabolismo
Interleucina-9/metabolismo
[Mh] Termos MeSH secundário: Síndrome Coronariana Aguda/imunologia
Síndrome Coronariana Aguda/metabolismo
Animais
Anticorpos Monoclonais/administração & dosagem
Aorta Torácica/imunologia
Aorta Torácica/patologia
Doenças da Aorta/genética
Doenças da Aorta/imunologia
Doenças da Aorta/patologia
Doenças da Aorta/prevenção & controle
Apolipoproteínas E/genética
Aterosclerose/genética
Aterosclerose/imunologia
Aterosclerose/patologia
Aterosclerose/prevenção & controle
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Células Cultivadas
Técnicas de Cocultura
Modelos Animais de Doenças
Progressão da Doença
Células Endoteliais/imunologia
Células Endoteliais/metabolismo
Seres Humanos
Interleucina-9/administração & dosagem
Interleucina-9/antagonistas & inibidores
Interleucina-9/genética
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Placa Aterosclerótica
Receptores de Interleucina-9/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Molécula 1 de Adesão de Célula Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Apolipoproteins E); 0 (IL9 protein, human); 0 (Il9r protein, mouse); 0 (Interleukin-9); 0 (Receptors, Interleukin-9); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (Vascular Cell Adhesion Molecule-1)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150515
[Lr] Data última revisão:
150515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150319
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvv110



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