Base de dados : MEDLINE
Pesquisa : A11.118.637.555.567.569.360 [Categoria DeCS]
Referências encontradas : 197 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 20 ir para página                         

  1 / 197 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28893952
[Au] Autor:Barik S; Miller MM; Cattin-Roy AN; Ukah TK; Chen W; Zaghouani H
[Ad] Endereço:Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO 65212.
[Ti] Título:IL-4/IL-13 Signaling Inhibits the Potential of Early Thymic Progenitors To Commit to the T Cell Lineage.
[So] Source:J Immunol;199(8):2767-2776, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Early thymic progenitors (ETPs) are endowed with diverse potencies and can give rise to myeloid and lymphoid lineage progenitors. How the thymic environment guides ETP commitment and maturation toward a specific lineage remains obscure. We have previously shown that ETPs expressing the heteroreceptor (HR) comprising IL-4Rα and IL-13Rα1 give rise to myeloid cells but not T cells. In this article, we show that signaling through the HR inhibits ETP maturation to the T cell lineage but enacts commitment toward the myeloid cells. Indeed, HR ETPs, but not HR ETPs, exhibit activated STAT6 transcription factor, which parallels with downregulation of Notch1, a critical factor for T cell development. Meanwhile, the myeloid-specific transcription factor C/EBPα, usually under the control of Notch1, is upregulated. Furthermore, in vivo inhibition of STAT6 phosphorylation restores Notch1 expression in HR ETPs, which regain T lineage potential. In addition, upon stimulation with IL-4 or IL-13, HR ETPs expressing virally transduced HR also exhibit STAT6 phosphorylation and downregulation of Notch1, leading to inhibition of lymphoid, but not myeloid, lineage potential. These observations indicate that environmental cytokines play a role in conditioning ETP lineage choice, which would impact T cell development.
[Mh] Termos MeSH primário: Subunidade alfa1 de Receptor de Interleucina-13/metabolismo
Interleucina-13/metabolismo
Interleucina-4/metabolismo
Células Precursoras de Linfócitos T/fisiologia
Receptores de Superfície Celular/metabolismo
Linfócitos T/fisiologia
Timo/imunologia
[Mh] Termos MeSH secundário: Animais
Proteínas Estimuladoras de Ligação a CCAAT/metabolismo
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Subunidade alfa1 de Receptor de Interleucina-13/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Mieloides/fisiologia
Receptores de Superfície Celular/genética
Fator de Transcrição STAT6/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Proteins); 0 (CEBPA protein, mouse); 0 (Il13ra1 protein, mouse); 0 (Il4ra protein, mouse); 0 (Interleukin-13); 0 (Interleukin-13 Receptor alpha1 Subunit); 0 (Receptors, Cell Surface); 0 (STAT6 Transcription Factor); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700498


  2 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28877990
[Au] Autor:Garreau A; Blaize G; Argenty J; Rouquié N; Tourdès A; Wood SA; Saoudi A; Lesourne R
[Ad] Endereço:Centre de Physiopathologie de Toulouse Purpan, Université de Toulouse, CNRS, INSERM, UPS, 31024 Toulouse, France; and.
[Ti] Título:Grb2-Mediated Recruitment of USP9X to LAT Enhances Themis Stability following Thymic Selection.
[So] Source:J Immunol;199(8):2758-2766, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Themis is a new component of the TCR signaling machinery that plays a critical role during T cell development. The positive selection of immature CD4 CD8 double-positive thymocytes and their commitment to the CD4 CD8 single-positive stage are impaired in mice, suggesting that Themis might be important to sustain TCR signals during these key developmental processes. However, the analysis of Themis mRNA levels revealed that gene expression is rapidly extinguished during positive selection. We show in this article that Themis protein expression is increased in double-positive thymocytes undergoing positive selection and is sustained in immature single-positive thymocytes, despite the strong decrease in Themis mRNA levels in these subsets. We found that Themis stability is controlled by the ubiquitin-specific protease USP9X, which removes ubiquitin K48-linked chains on Themis following TCR engagement. Biochemical analyses indicate that USP9X binds directly to the N-terminal CABIT domain of Themis and indirectly to the adaptor protein Grb2, with the latter interaction enabling recruitment of Themis/USP9X complexes to LAT, thereby sustaining Themis expression following positive selection. Together, these data suggest that TCR-mediated signals enhance Themis stability upon T cell development and identify USP9X as a key regulator of Themis protein turnover.
[Mh] Termos MeSH primário: Endopeptidases/metabolismo
Células Precursoras de Linfócitos T/fisiologia
Proteínas/metabolismo
Linfócitos T/fisiologia
Timo/imunologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Diferenciação Celular
Células Cultivadas
Seleção Clonal Mediada por Antígeno
Proteína Adaptadora GRB2/metabolismo
Ativação Linfocitária
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fosfoproteínas/metabolismo
Ligação Proteica
Estabilidade Proteica
Proteínas/genética
Receptores de Antígenos de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (GRB2 Adaptor Protein); 0 (Grb2 protein, mouse); 0 (Lat protein, mouse); 0 (Membrane Proteins); 0 (Phosphoproteins); 0 (Proteins); 0 (Receptors, Antigen, T-Cell); 0 (themis protein, mouse); EC 3.4.- (Endopeptidases); EC 3.4.99.- (Usp9x protein, mouse)
[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:170908
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700566


  3 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28864473
[Au] Autor:Desai P; Abboud G; Stanfield J; Thomas PG; Song J; Ware CF; Croft M; Salek-Ardakani S
[Ad] Endereço:Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL 32603.
[Ti] Título:HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity.
[So] Source:J Immunol;199(8):2968-2975, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mucosal immunity to reinfection with a highly virulent virus requires the accumulation and persistence of memory CD8 T cells at the site of primary infection. These cells may derive from memory precursor effector cells (MPECs), which are distinct from short-lived effector cells that provide acute protection but are often destined to die. Using respiratory virus infection, we show that herpes virus entry mediator (HVEM; TNFRSF14), a member of the TNF receptor superfamily, provides key signals for MPEC persistence. HVEM-deficient CD8 T cells expanded normally but were skewed away from MPECs with resultant poor development of circulating and lung-resident memory cells. HVEM was selectively expressed on MPECs whereas MPECs deficient in HVEM failed to survive in adoptive transfer recipients. As a consequence, HVEM-deficient recipients failed to afford protection against respiratory reinfection with influenza virus. HVEM therefore represents a critical signal for MPECs and development of protective mucosal CD8 T cell memory.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Vírus da Influenza A/imunologia
Infecções por Orthomyxoviridae/imunologia
Células Precursoras de Linfócitos T/imunologia
Membro 14 de Receptores do Fator de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos T CD8-Positivos/virologia
Autorrenovação Celular
Células Cultivadas
Modelos Animais de Doenças
Feminino
Imunidade nas Mucosas
Memória Imunológica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Células Precursoras de Linfócitos T/virologia
Membro 14 de Receptores do Fator de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Tumor Necrosis Factor, Member 14); 0 (Tnfrsf14 protein, mouse)
[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:170903
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700959


  4 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28551327
[Au] Autor:Dorfman DM; Morgan EA; Pelton A; Unitt C
[Ad] Endereço:Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Electronic address: ddorfman@partners.org.
[Ti] Título:T-cell transcription factor GATA-3 is an immunophenotypic marker of acute leukemias with T-cell differentiation.
[So] Source:Hum Pathol;65:166-174, 2017 Jul.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T-cell transcription factor GATA-3, known to play a role in early T-cell development and in the development of T-cell neoplasms, is expressed at high levels in fetal and adult thymus, as well as in acute leukemias with T-cell differentiation, including T-lymphoblastic leukemia/lymphoma (22/22 cases), early T-cell precursor lymphoblastic leukemia (11/11 cases), and mixed-phenotype acute leukemia, T/myeloid (4/5 cases), but only rarely in acute myeloid leukemia/myeloid sarcoma (1/36 cases), and not in B-lymphoblastic leukemia (0/16 cases). In contrast, T-bet, the other T-cell transcription factor that controls Th1/Th2 T-cell fate, is not expressed to any significant extent in immature thymocytes or in cases of T-lymphoblastic leukemia or acute myeloid leukemia/myeloid sarcoma, but is expressed in most cases (15/16) of B-lymphoblastic leukemia and in mixed-phenotype acute leukemia, B/myeloid. GATA-3-positive acute leukemias with T-cell differentiation were also found to express proto-oncogene C-MYC, in an average of 52% of neoplastic cells, which, along with GATA-3, may contribute to leukemogenesis, as suggested by transgenic mouse models. We conclude that GATA-3 is a sensitive and specific marker for the diagnosis of acute leukemias with T-cell differentiation and may be a useful addition to the panel of immunophenotypic markers for the diagnostic evaluation of acute leukemias.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Diferenciação Celular
Fator de Transcrição GATA3/análise
Células Precursoras de Linfócitos T/imunologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Criança
Diagnóstico Diferencial
Feminino
Seres Humanos
Imuno-Histoquímica
Imunofenotipagem/métodos
Masculino
Meia-Idade
Fenótipo
Células Precursoras de Linfócitos T/patologia
Leucemia-Linfoma Linfoblástico de Células T Precursoras/patologia
Valor Preditivo dos Testes
Proteínas Proto-Oncogênicas c-myc/análise
Reprodutibilidade dos Testes
Proteínas com Domínio T-Box/análise
Timócitos/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (GATA3 Transcription Factor); 0 (GATA3 protein, human); 0 (MYC protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


  5 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28530714
[Au] Autor:Ruscher R; Kummer RL; Lee YJ; Jameson SC; Hogquist KA
[Ad] Endereço:The Department of Laboratory Medicine and Pathology and Center for Immunology, University of Minnesota, Minneapolis, Minnesota, USA.
[Ti] Título:CD8αα intraepithelial lymphocytes arise from two main thymic precursors.
[So] Source:Nat Immunol;18(7):771-779, 2017 Jul.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TCRαß CD4 CD8α CD8ß intestinal intraepithelial lymphocytes (CD8αα IELs) are an abundant population of thymus-derived T cells that protect the gut barrier surface. We sought to better define the thymic IEL precursor (IELp) through analysis of its maturation, localization and emigration. We defined two precursor populations among TCRß CD4 CD8 thymocytes by dependence on the kinase TAK1 and rigorous lineage-exclusion criteria. Those IELp populations included a nascent PD-1 population and a T-bet population that accumulated with age. Both gave rise to intestinal CD8αα IELs after adoptive transfer. The PD-1 IELp population included more strongly self-reactive clones and was largely restricted by classical major histocompatibility complex (MHC) molecules. Those cells localized to the cortex and efficiently emigrated in a manner dependent on the receptor S1PR1. The T-bet IELp population localized to the medulla, included cells restricted by non-classical MHC molecules and expressed the receptor NK1.1, the integrin CD103 and the chemokine receptor CXCR3. The two IELp populations further differed in their use of the T cell antigen receptor (TCR) α-chain variable region (V ) and ß-chain variable region (V ). These data provide a foundation for understanding the biology of CD8αα IELs.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Mucosa Intestinal/imunologia
Células Precursoras de Linfócitos T/imunologia
Timócitos/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Transferência Adotiva
Animais
Antígenos CD
Antígenos Ly/imunologia
Antígenos CD8/imunologia
Linhagem da Célula
Movimento Celular/imunologia
Citometria de Fluxo
Imunofluorescência
Antígenos de Histocompatibilidade/imunologia
Imunidade nas Mucosas/imunologia
Cadeias alfa de Integrinas
Mucosa Intestinal/citologia
Linfócitos
Camundongos
Subfamília B de Receptores Semelhantes a Lectina de Células NK/imunologia
Fenótipo
Receptor de Morte Celular Programada 1/imunologia
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Receptores CXCR3
Receptores de Lisoesfingolipídeo/imunologia
Proteínas com Domínio T-Box/imunologia
Timócitos/citologia
Timo/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Ly); 0 (CD8 Antigens); 0 (CD8 antigen, alpha chain); 0 (Cxcr3 protein, mouse); 0 (Histocompatibility Antigens); 0 (Integrin alpha Chains); 0 (Klrb1c protein, mouse); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Receptors, CXCR3); 0 (Receptors, Lysosphingolipid); 0 (S1PR1 protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 0 (alpha E integrins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3751


  6 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27992401
[Au] Autor:Kitagawa Y; Ohkura N; Kidani Y; Vandenbon A; Hirota K; Kawakami R; Yasuda K; Motooka D; Nakamura S; Kondo M; Taniuchi I; Kohwi-Shigematsu T; Sakaguchi S
[Ad] Endereço:Department of Experimental Immunology, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
[Ti] Título:Guidance of regulatory T cell development by Satb1-dependent super-enhancer establishment.
[So] Source:Nat Immunol;18(2):173-183, 2017 Feb.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most Foxp3 regulatory T (T ) cells develop in the thymus as a functionally mature T cell subpopulation specialized for immune suppression. Their cell fate appears to be determined before Foxp3 expression; yet molecular events that prime Foxp3 T precursor cells are largely obscure. We found that T cell-specific super-enhancers (T -SEs), which were associated with Foxp3 and other T cell signature genes, began to be activated in T precursor cells. T cell-specific deficiency of the genome organizer Satb1 impaired T -SE activation and the subsequent expression of T signature genes, causing severe autoimmunity due to T cell deficiency. These results suggest that Satb1-dependent T -SE activation is crucial for T cell lineage specification in the thymus and that its perturbation is causative of autoimmune and other immunological diseases.
[Mh] Termos MeSH primário: Diferenciação Celular/imunologia
Fatores de Transcrição Forkhead/metabolismo
Proteínas de Ligação à Região de Interação com a Matriz/metabolismo
Linfócitos T Reguladores/fisiologia
Ativação Transcricional/imunologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Linhagem da Célula
Células Cultivadas
Elementos Facilitadores Genéticos/genética
Epigênese Genética
Fatores de Transcrição Forkhead/genética
Tolerância Imunológica
Masculino
Proteínas de Ligação à Região de Interação com a Matriz/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Especificidade de Órgãos
Células Precursoras de Linfócitos T/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Matrix Attachment Region Binding Proteins); 0 (Satb1 protein, mouse)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161220
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3646


  7 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27925658
[Au] Autor:von Muenchow L; Tsapogas P; Albertí-Servera L; Capoferri G; Doelz M; Rolink H; Bosco N; Ceredig R; Rolink AG
[Ad] Endereço:Developmental and Molecular Immunology, Department of Biomedicine, University of Basel, Basel, Switzerland.
[Ti] Título:Pro-B cells propagated in stromal cell-free cultures reconstitute functional B-cell compartments in immunodeficient mice.
[So] Source:Eur J Immunol;47(2):394-405, 2017 Feb.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Up to now long-term in vitro growth of pro-B cells was thought to require stromal cells. However, here we show that fetal liver (FL) and bone marrow (BM) derived pro-B cells can be propagated long-term in stromal cell-free cultures supplemented with IL-7, stem cell factor and FLT3 ligand. Within a week, most cells expressed surface CD19, CD79A, λ5, and VpreB antigens and had rearranged immunoglobulin D-J heavy chain genes. Both FL and BM pro-B cells reconstituted the B-cell compartments of immuno-incompetent Rag2-deficient mice, with FL pro-B cells generating follicular, marginal zone (MZB) and B1a B cells, and BM pro-B cells giving rise mainly to MZB cells. Reconstituted Rag2-deficient mice generated significant levels of IgM and IgG antibodies to a type II T-independent antigen; mice reconstituted with FL pro-B cells generated surprisingly high IgG titers. Finally, we show for the first time that mice reconstituted with mixtures of pro-B and pro-T cells propagated in stromal cell-free in vitro cultures mounted a T-cell-dependent antibody response. This novel stromal cell-free culture system facilitates our understanding of B-cell development and might be applied clinically.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Células da Medula Óssea/imunologia
Células Precursoras de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Animais
Formação de Anticorpos
Diferenciação Celular
Proliferação Celular
Células Cultivadas
Proteínas de Ligação a DNA/genética
Interleucina-7/metabolismo
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Precursoras de Linfócitos T/imunologia
Fator de Células-Tronco/metabolismo
Células Estromais/imunologia
Quimeras de Transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Interleukin-7); 0 (Membrane Proteins); 0 (Rag2 protein, mouse); 0 (Stem Cell Factor); 0 (flt3 ligand protein)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646638


  8 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27869820
[Au] Autor:Tsagaratou A; González-Avalos E; Rautio S; Scott-Browne JP; Togher S; Pastor WA; Rothenberg EV; Chavez L; Lähdesmäki H; Rao A
[Ad] Endereço:Department of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, California, USA.
[Ti] Título:TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells.
[So] Source:Nat Immunol;18(1):45-53, 2017 Jan.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TET proteins oxidize 5-methylcytosine in DNA to 5-hydroxymethylcytosine and other oxidation products. We found that simultaneous deletion of Tet2 and Tet3 in mouse CD4 CD8 double-positive thymocytes resulted in dysregulated development and proliferation of invariant natural killer T cells (iNKT cells). Tet2-Tet3 double-knockout (DKO) iNKT cells displayed pronounced skewing toward the NKT17 lineage, with increased DNA methylation and impaired expression of genes encoding the key lineage-specifying factors T-bet and ThPOK. Transfer of purified Tet2-Tet3 DKO iNKT cells into immunocompetent recipient mice resulted in an uncontrolled expansion that was dependent on the nonclassical major histocompatibility complex (MHC) protein CD1d, which presents lipid antigens to iNKT cells. Our data indicate that TET proteins regulate iNKT cell fate by ensuring their proper development and maturation and by suppressing aberrant proliferation mediated by the T cell antigen receptor (TCR).
[Mh] Termos MeSH primário: Diferenciação Celular
Proteínas de Ligação a DNA/metabolismo
Células T Matadoras Naturais/fisiologia
Células Precursoras de Linfócitos T/fisiologia
Proteínas Proto-Oncogênicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos CD1d/genética
Antígenos CD1d/metabolismo
Antígenos CD4/metabolismo
Antígenos CD8/metabolismo
Linhagem da Célula
Proliferação Celular
Células Cultivadas
Metilação de DNA/genética
Proteínas de Ligação a DNA/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Proto-Oncogênicas/genética
Receptores de Antígenos de Linfócitos T/metabolismo
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (CD1d antigen, mouse); 0 (CD4 Antigens); 0 (CD8 Antigens); 0 (DNA-Binding Proteins); 0 (Proto-Oncogene Proteins); 0 (Receptors, Antigen, T-Cell); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 0 (Tet2 protein, mouse); 0 (Tet3 protein, mouse); 0 (Th-POK protein, mouse); 0 (Transcription Factors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161122
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3630


  9 / 197 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27842955
[Au] Autor:Krueger A; Zietara N; Lyszkiewicz M
[Ad] Endereço:Institute of Molecular Medicine, Goethe University Frankfurt am Main, 60590 Frankfurt am Main, Germany. Electronic address: andreas.krueger@kgu.de.
[Ti] Título:T Cell Development by the Numbers.
[So] Source:Trends Immunol;38(2):128-139, 2017 Feb.
[Is] ISSN:1471-4981
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:T cells are continually generated in the thymus in a highly dynamic process comprising discrete steps of lineage commitment, T cell receptor (TCR) gene rearrangement, and selection. These steps are linked to distinct rates of proliferation, survival, and cell death, but a quantitative picture of T cell development is only beginning to emerge. Here we summarize recent technical advances, including genetic fate mapping, barcoding, and molecular timers, that have allowed the implementation of computational models to quantify developmental dynamics in the thymus. Coupling new techniques with mathematical models has recently resulted in the emergence of new paradigms in early hematopoiesis and might similarly open new perspectives on T cell development.
[Mh] Termos MeSH primário: Diferenciação Celular
Modelos Teóricos
Células Precursoras de Linfócitos T/fisiologia
Linfócitos T/fisiologia
Timo/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Hematopoese
Seres Humanos
Imunoensaio
Ativação Linfocitária
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


  10 / 197 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27759161
[Au] Autor:Fu G; Yu M; Chen Y; Zheng Y; Zhu W; Newman DK; Wang D; Wen R
[Ad] Endereço:The Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI, USA.
[Ti] Título:Phospholipase Cγ1 is required for pre-TCR signal transduction and pre-T cell development.
[So] Source:Eur J Immunol;47(1):74-83, 2017 Jan.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Pre-T cell receptor (TCR) signaling is required for pre-T cell survival, proliferation, and differentiation from the CD4 and CD8 double negative (DN) to the double positive (DP) stage. However, the pre-TCR signal transduction pathway is not fully understood and the signaling molecules involved have not been completely identified. Phospholipase Cγ (PLCγ) 1 is an important signaling molecule that generates two second messengers, diacylglycerol and inositol 1,4,5-trisphosphate, that are important to mediate PKC activation and intracellular Ca flux in many signaling pathways. Previously, we have shown that PLCγ1 is important for TCR-mediated signaling, development and T-cell activation, but the role of PLCγ1 in pre-TCR signal transduction and pre-T cell development is not known. In this study, we demonstrated that PLCγ1 expression level in pre-T cells was comparable to that in mature T cells. Deletion of PLCγ1 prior to the pre-TCR signaling stage partially blocked the DN3 to DN4 transition and reduced thymic cellularity. We also demonstrated that deletion of PLCγ1 impaired pre-T cell proliferation without affecting cell survival. Further study showed that deficiency of PLCγ1 impaired pre-TCR mediated Ca flux and Erk activation. Thus our studies demonstrate that PLCγ1 is important for pre-TCR mediated signal transduction and pre-T cell development.
[Mh] Termos MeSH primário: Diferenciação Celular
Fosfolipase C gama/metabolismo
Células Precursoras de Linfócitos T/citologia
Células Precursoras de Linfócitos T/metabolismo
Receptores de Antígenos de Linfócitos T/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Cálcio/metabolismo
Diferenciação Celular/genética
Diferenciação Celular/imunologia
Proliferação Celular
Sobrevivência Celular/genética
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Expressão Gênica
Genótipo
Ativação Linfocitária/genética
Ativação Linfocitária/imunologia
Camundongos
Camundongos Transgênicos
Fosfolipase C gama/deficiência
Fosfolipase C gama/genética
Fosforilação
Células Precursoras de Linfócitos T/imunologia
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/metabolismo
Timócitos/citologia
Timócitos/imunologia
Timócitos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Receptors, Antigen, T-Cell); 0 (Receptors, Antigen, T-Cell, alpha-beta); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.1.4.3 (Phospholipase C gamma); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646522



página 1 de 20 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde