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  1 / 2545 MEDLINE  
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[PMID]:29224228
[Au] Autor:Xu X; Sun Q; Mei Y; Liu Y; Zhao L
[Ad] Endereço:College of Basic Medicine and Biological Sciences, Medical Department, Soochow University, Suzhou, China.
[Ti] Título:Newcastle disease virus co-expressing interleukin 7 and interleukin 15 modified tumor cells as a vaccine for cancer immunotherapy.
[So] Source:Cancer Sci;109(2):279-288, 2018 Feb.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Interleukin 15 (IL15) and IL7 are two cytokines essential for T cell development and homeostasis. In order to improve the antitumor activity by Newcastle disease virus (NDV)-modified tumor vaccine, we generated a recombinant NDV co-expressing IL15 and IL7 (LX/IL(15+7)) through incorporation of a 2A self-processing peptide into IL15 and IL7 using reverse genetics. B16 cells infected with LX/IL(15+7) expressed both IL15 and IL7 stably. The cytotoxicity assay showed that murine melanoma cells modified with LX/IL(15+7) could significantly enhance the antitumor immune response in vitro. Then, the antitumor effects of tumor vaccine modified with recombinant virus were tested in the murine tumor models. We observed strong antitumor responses induced by LX/IL(15+7)-modified tumor cells both in prophylaxis and therapeutic models. Although the tumor-infiltrating CD4 T cells and CD8 T cells were both increased, the antitumor activity of the tumor vaccine modified with LX/IL(15+7) was dependent on CD8 T cells. Taken together, our data strongly indicated that tumor vaccine modified with NDV strain LX/IL(15+7) is a promising agent for cancer immunotherapy.
[Mh] Termos MeSH primário: Interleucina-15/metabolismo
Interleucina-7/metabolismo
Melanoma Experimental/terapia
Vírus da Doença de Newcastle/genética
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD8-Positivos/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Sobrevivência Celular
Vetores Genéticos/administração & dosagem
Imunoterapia
Interleucina-15/genética
Interleucina-7/genética
Melanoma Experimental/imunologia
Camundongos
Vírus da Doença de Newcastle/crescimento & desenvolvimento
Genética Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-15); 0 (Interleukin-7)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171211
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13468


  2 / 2545 MEDLINE  
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[PMID]:29236393
[Au] Autor:Lutsenko TN; Kovalenko MV; Galkin OY
[Ti] Título:Validation of biological activity testing procedure of recombinant human interleukin-7.
[So] Source:Ukr Biochem J;89(1):82-9, 2017 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Validation procedure for method of monitoring the biological activity of reсombinant human interleukin-7 has been developed and conducted according to the requirements of national and international recommendations. This method is based on the ability of recombinant human interleukin-7 to induce proliferation of T lymphocytes. It has been shown that to control the biological activity of recombinant human interleukin-7 peripheral blood mononuclear cells (PBMCs) derived from blood or cell lines can be used. Validation charac­teristics that should be determined depend on the method, type of product or object test/measurement and biological test systems used in research. The validation procedure for the method of control of biological activity of recombinant human interleukin-7 in peripheral blood mononuclear cells showed satisfactory results on all parameters tested such as specificity, accuracy, precision and linearity.
[Mh] Termos MeSH primário: Bioensaio/normas
Interleucina-7/farmacologia
Fito-Hemaglutininas/farmacologia
Linfócitos T/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Separação Celular/métodos
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/imunologia
Ativação Linfocitária/efeitos dos fármacos
Camundongos
Cultura Primária de Células
Proteínas Recombinantes/farmacologia
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
Linfócitos T/citologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (IL7 protein, human); 0 (Interleukin-7); 0 (Phytohemagglutinins); 0 (Recombinant Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj89.01.082


  3 / 2545 MEDLINE  
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[PMID]:29261677
[Au] Autor:Steele AK; Carrasco-Medina L; Sodora DL; Crawley AM
[Ad] Endereço:Center for Infectious Disease Research, Seattle, WA, United States of America.
[Ti] Título:Increased soluble IL-7 receptor concentrations associate with improved IL-7 therapy outcomes in SIV-infected ART-treated Rhesus macaques.
[So] Source:PLoS One;12(12):e0188427, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The use of interleukin-7 (IL-7) as an immunorestorative therapeutic has proven effective in HIV infection, cancer and bone marrow transplantation. Mediating its activity through membrane-bound IL-7 receptor α (mCD127), IL-7 therapy increases T-cell numbers and survival. A soluble form, sCD127, is found in plasma, and we have previously identified increased plasma sCD127 concentrations in HIV infection. Furthermore, patients with high sCD127 exhibited the best viral control, implicating a role for IL-7 or sCD127 directly in improved virologic/immunologic outcomes. The role of the cytokine IL-7 in elevating sCD127 levels was addressed here through assessment of retrospective samples obtained from SIV-infected antiretroviral (ART)-treated Rhesus macaques. IL-7 was administered in clustered weekly doses, allowing for an assessment prior, during and following IL-7 administration. The levels of sCD127 remained relatively unchanged during both early SIV infection and following initiation of ART. However, treatment with IL-7 increased sCD127 concentrations in most animals, transiently or persistently, paralleling increased T-cell numbers, correlating significantly with CD8+ T-cell levels. In addition, proliferating CD4+ or CD8+ T-cells (measured by Ki67) increased in association with elevated sCD127 concentrations. Finally, a high concentration of sCD127 in IL7-treated animals was associated with increased retention of T-cells (measured by BrDU). In addition, a lack, or loss of viral control was associated with more pronounced and frequent elevations in plasma sCD127 concentrations with IL-7 therapy. In summary, plasma sCD127 levels in SIV-infected ART-treated macaques was associated with therapeutic IL-7 administration, with higher sCD127 levels in macaques demonstrating the best T-cell responses. This study furthers our knowledge regarding the interrelationship between increased IL-7 levels and elevated sCD127 levels that may have implications for future IL-7 immunotherapeutic approaches in HIV-infected patients.
[Mh] Termos MeSH primário: Antirretrovirais/uso terapêutico
Interleucina-7/uso terapêutico
Receptores de Interleucina-7/metabolismo
Síndrome de Imunodeficiência Adquirida dos Símios/tratamento farmacológico
Síndrome de Imunodeficiência Adquirida dos Símios/virologia
Vírus da Imunodeficiência Símia/fisiologia
[Mh] Termos MeSH secundário: Animais
Antirretrovirais/farmacologia
Linfócitos T CD8-Positivos/imunologia
Sobrevivência Celular/imunologia
Interleucina-7/administração & dosagem
Interleucina-7/farmacologia
Ativação Linfocitária/imunologia
Contagem de Linfócitos
Macaca mulatta
Receptores de Interleucina-7/sangue
Síndrome de Imunodeficiência Adquirida dos Símios/sangue
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
Vírus da Imunodeficiência Símia/efeitos dos fármacos
Solubilidade
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Retroviral Agents); 0 (Interleukin-7); 0 (Receptors, Interleukin-7); 0 (interleukin-7 receptor, alpha chain)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188427


  4 / 2545 MEDLINE  
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[PMID]:29261670
[Au] Autor:Jeffery HC; McDowell P; Lutz P; Wawman RE; Roberts S; Bagnall C; Birtwistle J; Adams DH; Oo YH
[Ad] Endereço:Centre for Liver Research and National Institute for Health Research Birmingham Biomedical Research Centre, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
[Ti] Título:Human intrahepatic ILC2 are IL-13positive amphiregulinpositive and their frequency correlates with model of end stage liver disease score.
[So] Source:PLoS One;12(12):e0188649, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Innate lymphoid cells (ILC) have been implicated in the initiation of inflammation and fibrosis in mice. However, ILC have not been characterized in inflamed human liver tissue. METHODS: Human intrahepatic lymphocytes were isolated by mechanical digestion and phenotyped by flow cytometry. Conditioned medium from cultures of primary human biliary epithelial cells, stellate cells, fibroblasts and inflamed human liver tissue was used to model the effects of the inflammatory liver environment of ILC phenotype and function. RESULTS: All three ILC subsets were present in the human liver, with the ILC1 (CRTH2negCD117neg) subset constituting around 70% of intrahepatic ILCs. Both NCRpos (NKp44+) and NCRneg ILC3 (CRTH2negCD117pos) subsets were also detected. ILC2 (CRTH2pos) frequency correlated with disease severity measured by model of end stage liver disease (MELD) scoring leading us to study this subset in more detail. ILC2 displayed a tissue resident CD69+ CD161++ phenotype and expressed chemokine receptor CCR6 allowing them to respond to CCL20 secreted by cholangiocytes and stellate cells. ILC2 expressed integrins VLA-5 and VLA-6 and the IL-2 and IL-7 cytokine receptors CD25 and CD127 although IL-2 and IL-7 were barely detectable in inflamed liver tissue. Although biliary epithelial cells secrete IL-33, intrahepatic ILC2 had low expression of the ST2 receptor. Intrahepatic ILC2 secreted the immunoregulatory and repair cytokines IL-13 and amphiregulin. CONCLUSIONS: Intrahepatic ILC2 express receptors allowing them to be recruited to bile ducts in inflamed portal tracts. Their frequencies increased with worsening liver function. Their secretion of IL-13 and amphiregulin suggests they may be recruited to promote resolution and repair and thereby they may contribute to ongoing fibrogenesis in liver disease.
[Mh] Termos MeSH primário: Anfirregulina/metabolismo
Doença Hepática Terminal/imunologia
Imunidade Inata
Interleucina-13/metabolismo
Fígado/metabolismo
Linfócitos/metabolismo
Modelos Biológicos
[Mh] Termos MeSH secundário: Células Epiteliais/metabolismo
Seres Humanos
Inflamação/patologia
Integrinas/genética
Integrinas/metabolismo
Interleucina-2/metabolismo
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Interleucina-7/metabolismo
Fígado/patologia
Contagem de Linfócitos
Subfamília B de Receptores Semelhantes a Lectina de Células NK/metabolismo
Fenótipo
Receptores de Quimiocinas/genética
Receptores de Quimiocinas/metabolismo
Receptores Imunológicos/metabolismo
Receptores de Prostaglandina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amphiregulin); 0 (Integrins); 0 (Interleukin-13); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-7); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Receptors, Chemokine); 0 (Receptors, Immunologic); 0 (Receptors, Prostaglandin); 0 (prostaglandin D2 receptor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188649


  5 / 2545 MEDLINE  
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[PMID]:28904110
[Au] Autor:Ucar D; Márquez EJ; Chung CH; Marches R; Rossi RJ; Uyar A; Wu TC; George J; Stitzel ML; Palucka AK; Kuchel GA; Banchereau J
[Ad] Endereço:The Jackson Laboratory for Genomic Medicine, Farmington, CT duygu.ucar@jax.org.
[Ti] Título:The chromatin accessibility signature of human immune aging stems from CD8 T cells.
[So] Source:J Exp Med;214(10):3123-3144, 2017 Oct 02.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aging is linked to deficiencies in immune responses and increased systemic inflammation. To unravel the regulatory programs behind these changes, we applied systems immunology approaches and profiled chromatin accessibility and the transcriptome in PBMCs and purified monocytes, B cells, and T cells. Analysis of samples from 77 young and elderly donors revealed a novel and robust aging signature in PBMCs, with simultaneous systematic chromatin closing at promoters and enhancers associated with T cell signaling and a potentially stochastic chromatin opening mostly found at quiescent and repressed sites. Combined analyses of chromatin accessibility and the transcriptome uncovered immune molecules activated/inactivated with aging and identified the silencing of the gene and the IL-7 signaling pathway genes as potential biomarkers. This signature is borne by memory CD8 T cells, which exhibited an aging-related loss in binding of NF-κB and STAT factors. Thus, our study provides a unique and comprehensive approach to identifying candidate biomarkers and provides mechanistic insights into aging-associated immunodeficiency.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Linfócitos T CD8-Positivos/fisiologia
Cromatina/fisiologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Envelhecimento/imunologia
Biomarcadores
Linfócitos T CD8-Positivos/imunologia
Epigênese Genética
Feminino
Seres Humanos
Interleucina-7/fisiologia
Subunidade alfa de Receptor de Interleucina-7/fisiologia
Leucócitos Mononucleares/imunologia
Leucócitos Mononucleares/fisiologia
Masculino
Transdução de Sinais/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Chromatin); 0 (IL7 protein, human); 0 (IL7R protein, human); 0 (Interleukin-7); 0 (Interleukin-7 Receptor alpha Subunit)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20170416


  6 / 2545 MEDLINE  
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[PMID]:28893953
[Au] Autor:Kyoizumi S; Kubo Y; Kajimura J; Yoshida K; Hayashi T; Nakachi K; Moore MA; van den Brink MRM; Kusunoki Y
[Ad] Endereço:Department of Molecular Biosciences, Radiation Effects Research Foundation, Hiroshima 732-0815, Japan; kyoizumi@rerf.or.jp.
[Ti] Título:Fate Decision Between Group 3 Innate Lymphoid and Conventional NK Cell Lineages by Notch Signaling in Human Circulating Hematopoietic Progenitors.
[So] Source:J Immunol;199(8):2777-2793, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of Notch signaling in human innate lymphoid cell (ILC) differentiation is unclear, although IL-7 and IL-15 promote differentiation of natural cytotoxicity receptor (NCR) NKp44 group 3 ILCs (NCR ILC3s) and conventional NK (cNK) cells from CD34 hematopoietic progenitor cells (HPCs) ex vivo. In this study, we analyzed the functions of Notch in the differentiation of NCR ILC3s and cNK cells from human HPC subpopulations circulating in peripheral blood by limiting dilution and clonal assays using high-throughput flow cytometry. We demonstrated that Notch signaling in combination with IL-7 induced NCR ILC3 differentiation, but conversely suppressed IL-15-dependent cNK cell generation in CD45RA Flt-3 c-Kit , a novel innate lymphocyte-committed HPC subpopulation. In contrast, Notch signaling induced CD45RA Flt-3 c-Kit multipotent HPCs to generate CD34 CD7 CD62L , the earliest thymic progenitor-like cells, which preserved high cNK/T cell potential, but lost NCR ILC3 potential. These findings implicate the countervailing functions of Notch signaling in the fate decision between NCR ILC3 and cNK cell lineages at different maturational stages of human HPCs. Inhibition of Notch functions by Abs specific for either the Notch1 or Notch2 negative regulatory region suggested that both Notch1 and Notch2 signals were involved in the fate decision of innate lymphocyte-committed HPCs and in the generation of earliest thymic progenitor-like cells from multipotent HPCs. Furthermore, the synergistic interaction between Notch and IL-7 in NCR ILC3 commitment was primarily explicable by the induction of IL-7 receptor expression in the innate lymphocyte-committed HPCs by Notch stimulation, suggesting the pivotal role of Notch in the transcriptional control required for human NCR ILC3 commitment.
[Mh] Termos MeSH primário: Células-Tronco Hematopoéticas/fisiologia
Células Matadoras Naturais/fisiologia
Subpopulações de Linfócitos/fisiologia
Linfócitos/fisiologia
Receptores Notch/metabolismo
[Mh] Termos MeSH secundário: Antígenos CD34/metabolismo
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Seres Humanos
Imunidade Inata
Interleucina-15/metabolismo
Interleucina-7/metabolismo
Receptor 2 Desencadeador da Citotoxicidade Natural/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (Interleukin-15); 0 (Interleukin-7); 0 (NCR2 protein, human); 0 (Natural Cytotoxicity Triggering Receptor 2); 0 (Receptors, Notch)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601711


  7 / 2545 MEDLINE  
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[PMID]:28854279
[Au] Autor:Tanaka T; Watanabe S; Takahashi M; Sato K; Saida Y; Baba J; Arita M; Sato M; Ohtsubo A; Shoji S; Nozaki K; Ichikawa K; Kondo R; Aoki N; Ohshima Y; Sakagami T; Abe T; Moro H; Koya T; Tanaka J; Kagamu H; Yoshizawa H; Kikuchi T
[Ad] Endereço:Department of Respiratory Medicine and Infectious Diseases, Niigata University Graduate School of Medical and Dental Sciences, Niigata City, Niigata, Japan.
[Ti] Título:Transfer of in vitro-expanded naïve T cells after lymphodepletion enhances antitumor immunity through the induction of polyclonal antitumor effector T cells.
[So] Source:PLoS One;12(8):e0183976, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The adoptive transfer of effector T cells combined with lymphodepletion has demonstrated promising antitumor effects in mice and humans, although the availability of tumor-specific T cells is limited. We and others have also demonstrated that the transfer of polyclonal naïve T cells induces tumor-specific effector T cells and enhances antitumor immunity after lymphodepletion. Because tumors have been demonstrated to induce immunosuppressive networks and regulate the function of T cells, obtaining a sufficient number of fully functional naïve T cells that are able to differentiate into tumor-specific effector T cells remains difficult. To establish culture methods to obtain a large number of polyclonal T cells that are capable of differentiating into tumor-specific effector T cells, naïve T cells were activated with anti-CD3 mAbs in vitro. These cells were stimulated with IL-2 and IL-7 for the CD8 subset or with IL-7 and IL-23 for the CD4 subset. Transfer of these hyperexpanded T cells after lymphodepletion showed significant antitumor efficacy, and tumor-specific effector T cells were primed from these expanded T cells in tumor-bearing hosts. Moreover, these ex vivo-expanded T cells maintained T cell receptor diversity and showed long-term persistence of memory against specific tumors. Further analyses revealed that combination therapy consisting of vaccination with dendritic cells that were co-cultured with irradiated whole tumor cells and the transfer of ex vivo-expanded T cells significantly enhanced antitumor immunity. These results indicate that the transfer of ex vivo-expanded polyclonal T cells can be combined with other immunotherapies and augment antitumor effects.
[Mh] Termos MeSH primário: Transferência Adotiva/métodos
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/transplante
Neoplasias/terapia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD8-Positivos/citologia
Linfócitos T CD8-Positivos/imunologia
Técnicas de Cultura de Células
Linhagem Celular Tumoral
Proliferação Celular
Células Cultivadas
Células Dendríticas/imunologia
Células Dendríticas/transplante
Feminino
Interleucina-2/imunologia
Interleucina-23/imunologia
Interleucina-7/imunologia
Ativação Linfocitária
Depleção Linfocítica
Camundongos Endogâmicos C57BL
Neoplasias/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-2); 0 (Interleukin-23); 0 (Interleukin-7); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183976


  8 / 2545 MEDLINE  
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[PMID]:28825702
[Au] Autor:Berthault C; Ramond C; Burlen-Defranoux O; Soubigou G; Chea S; Golub R; Pereira P; Vieira P; Cumano A
[Ad] Endereço:Unit for Lymphopoiesis, Pasteur Institute, Paris, France. Immunology department.
[Ti] Título:Asynchronous lineage priming determines commitment to T cell and B cell lineages in fetal liver.
[So] Source:Nat Immunol;18(10):1139-1149, 2017 Oct.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular events that initiate lymphoid-lineage specification remain unidentified because the stages of differentiation during which lineage commitment occurs are difficult to characterize. We isolated fetal liver progenitor cells undergoing restriction of their differentiation potential toward the T cell-innate lymphoid cell lineage or the B cell lineage. Transcripts that defined the molecular signatures of these two subsets were sequentially upregulated in lympho-myeloid precursor cells and in common lymphoid progenitor cells, respectively, and this preceded lineage restriction; this indicates that T cell-versus-B cell commitment is not a binary fate 'decision'. The T cell-bias and B cell-bias transcriptional programs were frequently co-expressed in common lymphoid progenitor cells and were segregated in subsets biased toward T cell differentiation or B cell differentiation, after interleukin 7 (IL-7) signaling that controlled the number of progenitor cells engaging in T cell differentiation versus B cell differentiation.
[Mh] Termos MeSH primário: Linfócitos B/citologia
Linhagem da Célula
Fígado/citologia
Linfopoese
Linfócitos T/citologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/metabolismo
Biomarcadores
Diferenciação Celular/genética
Linhagem da Célula/genética
Análise por Conglomerados
Feto
Perfilação da Expressão Gênica
Regulação da Expressão Gênica no Desenvolvimento
Imunofenotipagem
Interleucina-7/metabolismo
Fígado/embriologia
Células Progenitoras Linfoides/citologia
Células Progenitoras Linfoides/metabolismo
Linfopoese/genética
Camundongos
Camundongos Transgênicos
Transdução de Sinais
Linfócitos T/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-7)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3820


  9 / 2545 MEDLINE  
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[PMID]:28821585
[Au] Autor:Lang MJ; Mori M; Ruer-Laventie J; Pieters J
[Ad] Endereço:Biozentrum, University of Basel, Basel 4056, Switzerland.
[Ti] Título:A Coronin 1-Dependent Decision Switch in Juvenile Mice Determines the Population of the Peripheral Naive T Cell Compartment.
[So] Source:J Immunol;199(7):2421-2431, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Following thymic maturation, T cells egress as recent thymic emigrants to peripheral lymphoid organs where they undergo an additional maturation step to mature naive T cells that circulate through secondary lymphoid organs ready to be activated upon pathogenic challenges. Thymic maturation and peripheral T cell survival depend on several signaling cascades, but whether a dedicated mechanism exists that exclusively regulates homeostasis of mature naive T cells without affecting thymocytes and/or recent thymic emigrants remains unknown. In this article, we provide evidence for a specific and exclusive role of the WD repeat containing protein coronin 1 in the maintenance of naive T cells in peripheral lymphoid organs. We show that coronin 1 is dispensable for thymocyte survival and development, egress from the thymus, and survival of recent thymic emigrants. Importantly, coronin 1-deficient mice possessed comparable levels of peripheral T cells within the first 2 wk after birth but failed to populate the peripheral T cell compartment at later stages. Furthermore, dendritic cell- and IL-2/7-dependent T cell survival was found to be independent of coronin 1. Together, these results suggest the existence of a hitherto unrecognized coronin 1-dependent decision switch early during life that is responsible for peripheral naive T cell survival and homeostasis.
[Mh] Termos MeSH primário: Sobrevivência Celular
Proteínas dos Microfilamentos/metabolismo
Subpopulações de Linfócitos T/fisiologia
Timo/citologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/fisiologia
Células Dendríticas/metabolismo
Homeostase
Interleucina-2/farmacologia
Interleucina-7/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Proteínas dos Microfilamentos/deficiência
Proteínas dos Microfilamentos/genética
Transdução de Sinais
Subpopulações de Linfócitos T/metabolismo
Timócitos/efeitos dos fármacos
Timócitos/fisiologia
Timo/anatomia & histologia
Timo/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-2); 0 (Interleukin-7); 0 (Microfilament Proteins); 145420-64-0 (coronin proteins)
[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.1700438


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[PMID]:28724580
[Au] Autor:Venet F; Demaret J; Blaise BJ; Rouget C; Girardot T; Idealisoa E; Rimmelé T; Mallet F; Lepape A; Textoris J; Monneret G
[Ad] Endereço:Immunology Laboratory, Hospices Civils de Lyon, Edouard Herriot Hospital, 69437 Lyon, France; fabienne.venet@chu-lyon.fr.
[Ti] Título:IL-7 Restores T Lymphocyte Immunometabolic Failure in Septic Shock Patients through mTOR Activation.
[So] Source:J Immunol;199(5):1606-1615, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T lymphocyte alterations are central to sepsis pathophysiology, whereas related mechanisms remain poorly understood. We hypothesized that metabolic alterations could play a role in sepsis-induced T lymphocyte dysfunction. Samples from septic shock patients were obtained at day 3 and compared with those from healthy donors. T cell metabolic status was evaluated in the basal condition and after T cell stimulation. We observed that basal metabolic content measured in lymphocytes by nuclear magnetic resonance spectroscopy was altered in septic patients. Basal ATP concentration, oxidative phosphorylation (OXPHOS), and glycolysis pathways in T cells were decreased as well. After stimulation, T lymphocytes from patients failed to induce glycolysis, OXPHOS, ATP production, GLUT1 expression, glucose entry, and proliferation to similar levels as controls. This was associated with significantly altered mTOR, but not Akt or HIF-1α, activation and only minor AMPKα phosphorylation dysfunction. IL-7 treatment improved mTOR activation, GLUT1 expression, and glucose entry in septic patients' T lymphocytes, leading to their enhanced proliferation. mTOR activation was central to this process, because rapamycin systematically inhibited the beneficial effect of recombinant human IL-7. We demonstrate the central role of immunometabolism and, in particular, mTOR alterations in the pathophysiology of sepsis-induced T cell alterations. Our results support the rationale for targeting metabolism in sepsis with recombinant human IL-7 as a treatment option.
[Mh] Termos MeSH primário: Glucose/metabolismo
Imunoterapia/métodos
Interleucina-7/imunologia
Choque Séptico/imunologia
Linfócitos T/imunologia
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Idoso
Idoso de 80 Anos ou mais
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Metabolismo Energético/efeitos dos fármacos
Feminino
Transportador de Glucose Tipo 1/genética
Transportador de Glucose Tipo 1/metabolismo
Glicólise/efeitos dos fármacos
Seres Humanos
Interleucina-7/uso terapêutico
Masculino
Meia-Idade
Ressonância Magnética Nuclear Biomolecular
Fosforilação Oxidativa/efeitos dos fármacos
Choque Séptico/terapia
Sirolimo/farmacologia
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 1); 0 (Interleukin-7); 0 (SLC2A1 protein, human); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); IY9XDZ35W2 (Glucose); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700127



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