Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.816.824.830 [Categoria DeCS]
Referências encontradas : 5792 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 580 ir para página                         

  1 / 5792 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28456719
[Au] Autor:Jansen MAE; van den Heuvel D; Jaddoe VWV; van Zelm MC; Moll HA
[Ad] Endereço:The Generation R Study Group, Erasmus MC-Sophia, Rotterdam, The Netherlands; Department of Pediatrics, Erasmus MC-Sophia, Rotterdam, The Netherlands; Department of Immunology, Erasmus University Medical Center (Erasmus MC), Rotterdam, The Netherlands.
[Ti] Título:Abnormalities in CD57+ cytotoxic T cells and Vδ1+ γδT cells in subclinical celiac disease in childhood are affected by cytomegalovirus. The Generation R Study.
[So] Source:Clin Immunol;183:233-239, 2017 10.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Celiac disease (CD) is a digestive and autoimmune disorder driven by an immune response to modified gluten peptides. Affected intestines show infiltrates of various T-cell and NK-cell subsets. It is currently unclear if individuals with subclinical CD have systemic abnormalities in immune cells. We here studied whether subclinical CD is associated with changes in blood CD57-expressing and Vδ1-expressing lymphocytes in children, and whether cytomegalovirus (CMV) infection modifies this association. Included were 1068 children from the Generation R Study. Serum Immunoglobulin G (IgG) levels against CMV were measured by ELISA; Tissue transglutaminase type 2 antibody (TG2A) levels with fluorescence enzyme immunoassay (FEIA). Duodenal biopsies, additional Human Leukocyte Antigen (HLA) DQ 2.2, 2.5 and 8 and endomysial antibody (EMA) typing were performed in TG2A positive children. Subclinical CD cases (n=12) had 1.8 fold (95% CI 1.06; 3.1) fewer Vδ1+ T cells which was predominantly observed in CMV seronegative children (p-interaction 0.02), and 2.7 fold (95% CI 1.25; 5.99) more CD57+ T cells than HLA DQ2/-DQ8 positive controls (n=339). Hence, children with subclinical CD have alterations in specific blood T cell subsets that are linked to viral pathology. The observed interaction effect between subclinical CD and CMV may contribute to the understanding of disease pathogenesis.
[Mh] Termos MeSH primário: Antígenos CD57/fisiologia
Doença Celíaca/imunologia
Infecções por Citomegalovirus/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/fisiologia
Linfócitos T Citotóxicos/fisiologia
[Mh] Termos MeSH secundário: Doença Celíaca/complicações
Criança
Pré-Escolar
Infecções por Citomegalovirus/complicações
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD57 Antigens); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


  2 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28461569
[Au] Autor:Peigné CM; Léger A; Gesnel MC; Konczak F; Olive D; Bonneville M; Breathnach R; Scotet E
[Ad] Endereço:Centre de Recherche en Cancérologie et Immunologie Nantes-Angers, INSERM, CNRS, Université d'Angers, Université de Nantes, 44035 Nantes, France.
[Ti] Título:The Juxtamembrane Domain of Butyrophilin BTN3A1 Controls Phosphoantigen-Mediated Activation of Human Vγ9Vδ2 T Cells.
[So] Source:J Immunol;198(11):4228-4234, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vγ9Vδ2 T lymphocytes are the major human peripheral γδ T cell subset, with broad reactivity against stressed human cells, including tumor cells. Vγ9Vδ2 T cells are specifically activated by small phosphorylated metabolites called phosphoantigens (PAg). Stress-induced changes in target cell PAg levels are specifically detected by butyrophilin (BTN)3A1, using its intracellular B30.2 domain. This leads to the activation of Vγ9Vδ2 T cells. In this study, we show that changes in the juxtamembrane domain of BTN3A1, but not its transmembrane domain, induce a markedly enhanced or reduced γδ T cell reactivity. There is thus a specific requirement for BTN3A1's juxtamembrane domain for correct γδ T cell-related function. This work identified, as being of particular importance, a juxtamembrane domain region of BTN3A molecules identified as a possible dimerization interface and that is located close to the start of the B30.2 domain.
[Mh] Termos MeSH primário: Antígenos CD/química
Antígenos CD/imunologia
Butirofilinas/química
Butirofilinas/imunologia
Ativação Linfocitária
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Subpopulações de Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígenos/química
Antígenos/imunologia
Antígenos CD/metabolismo
Butirofilinas/metabolismo
Células HEK293
Seres Humanos
Proteínas Mutantes Quiméricas/imunologia
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Antigens, CD); 0 (BTN3A1 protein, human); 0 (Butyrophilins); 0 (Mutant Chimeric Proteins); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601910


  3 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28741710
[Au] Autor:Duault C; Betous D; Bezombes C; Roga S; Cayrol C; Girard JP; Fournié JJ; Poupot M
[Ad] Endereço:INSERM UMR1037-Cancer Research Center of Toulouse, Toulouse, France.
[Ti] Título:IL-33-expanded human Vγ9Vδ2 T cells have anti-lymphoma effect in a mouse tumor model.
[So] Source:Eur J Immunol;47(12):2137-2141, 2017 Dec.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:From several years, the anticancer effects of Vγ9 T lymphocytes make these cells good candidates for cancer immunotherapies. However, the proved efficacy of γδ Τ cell-based cancer immunotherapies in some clinical trials was minimized due to the inherent toxicity of IL-2, which is essential for the combination therapy with Phosphoantigen (PAg). Recently, we showed that IL-33, a γ chain receptor-independent cytokine, was able to induce the in vitro proliferation of PAg-activated Vγ9 T cells, which were fully functional expressing IFN-γ and TNF-α and showing in vitro anti-tumor cytotoxicity. We proposed IL-33 as an alternative to IL-2 for Vγ9 T cell-based cancer immunotherapies, and have therefore evaluated the efficacy of this cytokine in preclinical investigations. This study shows that human Vγ9 T cells are able to proliferate in a mouse model with the combination of PAg and rhIL-33, and that IL-33-expanded Vγ9 T cells can prevent tumor growth in a mouse lymphoma model.
[Mh] Termos MeSH primário: Imunoterapia/métodos
Interleucina-33/farmacologia
Linfoma/tratamento farmacológico
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Linfócitos T/transplante
Ensaios Antitumorais Modelo de Xenoenxerto/métodos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células Cultivadas
Seres Humanos
Interleucina-33/genética
Linfoma/imunologia
Linfoma/metabolismo
Camundongos Endogâmicos NOD
Camundongos Knockout
Camundongos SCID
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Proteínas Recombinantes/farmacologia
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Carga Tumoral/efeitos dos fármacos
Carga Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL33 protein, human); 0 (Interleukin-33); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Recombinant Proteins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747093


  4 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468758
[Au] Autor:Djaoud Z; Guethlein LA; Horowitz A; Azzi T; Nemat-Gorgani N; Olive D; Nadal D; Norman PJ; Münz C; Parham P
[Ad] Endereço:Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305 zdjaoud@stanford.edu peropa@stanford.edu.
[Ti] Título:Two alternate strategies for innate immunity to Epstein-Barr virus: One using NK cells and the other NK cells and γδ T cells.
[So] Source:J Exp Med;214(6):1827-1841, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most humans become infected with Epstein-Barr virus (EBV), which then persists for life. Infrequently, EBV infection causes infectious mononucleosis (IM) or Burkitt lymphoma (BL). Type I EBV infection, particularly type I BL, stimulates strong responses of innate immune cells. Humans respond to EBV in two alternative ways. Of 24 individuals studied, 13 made strong NK and γδ T cell responses, whereas 11 made feeble γδ T cell responses but stronger NK cell responses. The difference does not correlate with sex, HLA type, or previous exposure to EBV or cytomegalovirus. Cohorts of EBV children and pediatric IM patients include both group 1 individuals, with high numbers of γδ T cells, and group 2 individuals, with low numbers. The even balance of groups 1 and 2 in the human population points to both forms of innate immune response to EBV having benefit for human survival. Correlating these distinctive responses with the progress of EBV infection might facilitate the management of EBV-mediated disease.
[Mh] Termos MeSH primário: Herpesvirus Humano 4/imunologia
Imunidade Inata
Células Matadoras Naturais/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Linfócitos B/imunologia
Linfócitos B/virologia
Butirofilinas/metabolismo
Diferenciação Celular/imunologia
Proliferação Celular
Citomegalovirus/fisiologia
Infecções por Vírus Epstein-Barr/imunologia
Infecções por Vírus Epstein-Barr/patologia
Infecções por Vírus Epstein-Barr/virologia
Genótipo
Antígenos HLA/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Fenótipo
Doadores de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (BTN3A1 protein, human); 0 (Butyrophilins); 0 (HLA Antigens); 0 (KLRK1 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171206
[Lr] Data última revisão:
171206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161017


  5 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28972090
[Au] Autor:Campbell JJ; Ebsworth K; Ertl LS; McMahon JP; Newland D; Wang Y; Liu S; Miao Z; Dang T; Zhang P; Charo IF; Singh R; Schall TJ
[Ad] Endereço:ChemoCentryx Inc., Mountain View, CA 94043 jcampbell@chemocentryx.com.
[Ti] Título:IL-17-Secreting γδ T Cells Are Completely Dependent upon CCR6 for Homing to Inflamed Skin.
[So] Source:J Immunol;199(9):3129-3136, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:mAbs that neutralize IL-17 or its receptor have proven efficacious in treating moderate-to-severe psoriasis, confirming IL-17 as an important driver of this disease. In mice, a rare population of T cells, γδT17 cells, appears to be a dominant source of IL-17 in experimental psoriasis. These cells traffic between lymph nodes and the skin, and are identified by their coexpression of the TCR variable regions γ4 and δ4. These cells are homologous to the Vγ9Vδ2 T cell population identified in human psoriatic plaques. In this study we report that a potent and specific small molecule antagonist of the CCR6 chemokine receptor, CCX2553, was efficacious in reducing multiple aspects of psoriasis in two different murine models of the disease. Administration of CCX2553 ameliorated skin inflammation in both the IL-23-induced ear swelling model and the topical imiquimod model, and significantly reduced the number of γδT17 cells in inflamed skin. γδT17 cells were greatly reduced in imiquimod-treated skin of CCR6 mice, but adoptively transferred wild-type (CCR6 ) γδT17 cells homed normally to the skin of imiquimod-treated CCR6 mice. Our data suggest that γδT17 cells are completely dependent on CCR6 for homing to psoriasiform skin. Thus, CCR6 may constitute a novel target for a mechanistically distinct therapeutic approach to treating psoriasis.
[Mh] Termos MeSH primário: Movimento Celular/imunologia
Interleucina-17/imunologia
Psoríase/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Receptores CCR6/imunologia
Pele/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Movimento Celular/efeitos dos fármacos
Movimento Celular/genética
Interleucina-17/genética
Subunidade p19 da Interleucina-23/genética
Subunidade p19 da Interleucina-23/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Knockout
Psoríase/genética
Psoríase/patologia
Receptores de Antígenos de Linfócitos T gama-delta/genética
Receptores CCR6/genética
Pele/patologia
Linfócitos T/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCR6 protein, mouse); 0 (Il23a protein, mouse); 0 (Interleukin-17); 0 (Interleukin-23 Subunit p19); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, CCR6)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700826


  6 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28954887
[Au] Autor:Gan PY; Fujita T; Ooi JD; Alikhan MA; Dick J; Shim R; Odobasic D; O'Sullivan KM; Kitching AR; Holdsworth SR
[Ad] Endereço:Centre for Inflammatory Diseases, Department of Medicine, Monash Medical Centre, Monash University, Clayton, Victoria 3168, Australia; Poh-yi.gan@monash.edu.
[Ti] Título:Pathogenic Role for γδ T Cells in Autoimmune Anti-Myeloperoxidase Glomerulonephritis.
[So] Source:J Immunol;199(9):3042-3050, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myeloperoxidase (MPO) anti-neutrophil cytoplasmic Ab (ANCA)-associated vasculitis results from autoimmunity to MPO. IL-17A plays a critical role in generating this form of autoimmune injury but its cell of origin is uncertain. We addressed the hypothesis that IL-17A-producing γδ T cells are a nonredundant requisite in the development of MPO autoimmunity and glomerulonephritis (GN). We studied MPO-ANCA GN in wild type, αß, or γδ T cell-deficient (C57BL/6, , and respectively) mice. Both T cell populations played important roles in the generation of autoimmunity to MPO and GN. Humoral autoimmunity was dependent on intact αß T cells but was unaffected by γδ T cell deletion. Following MPO immunization, activated γδ T cells migrate to draining lymph nodes. Studies in and transfer of γδ T cells to mice show that γδ T cells facilitate the generation of anti-MPO autoimmunity and GN. mice that received γδ T cells demonstrate that the development of anti-MPO autoimmunity and GN are dependent on γδ T cell IL-17A production. Finally, transfer of anti-MPO CD4 T cell clones to naive and wild type mice with planted glomerular MPO shows that γδ T cells are also necessary for recruitment of anti-MPO αß CD4 effector T cells. This study demonstrates that IL-17A produced by γδ T cells plays a critical role in the pathogenesis of MPO-ANCA GN by promoting the development of MPO-specific αß T cells.
[Mh] Termos MeSH primário: Doenças Autoimunes/imunologia
Linfócitos T CD4-Positivos/imunologia
Glomerulonefrite/imunologia
Peroxidase/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
[Mh] Termos MeSH secundário: Animais
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/genética
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/imunologia
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/patologia
Autoanticorpos/genética
Autoanticorpos/imunologia
Doenças Autoimunes/genética
Doenças Autoimunes/patologia
Linfócitos T CD4-Positivos/patologia
Glomerulonefrite/genética
Glomerulonefrite/patologia
Interleucina-17/genética
Interleucina-17/imunologia
Camundongos
Camundongos Knockout
Peroxidase/genética
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Il17a protein, mouse); 0 (Interleukin-17); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Receptors, Antigen, T-Cell, gamma-delta); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602025


  7 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28855314
[Au] Autor:Muschaweckh A; Petermann F; Korn T
[Ad] Endereço:Klinikum Rechts der Isar, Neurologische Klinik, Technische Universität München, 81675 Munich, Germany; and.
[Ti] Título:IL-1ß and IL-23 Promote Extrathymic Commitment of CD27 CD122 γδ T Cells to γδT17 Cells.
[So] Source:J Immunol;199(8):2668-2679, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:γδT17 cells are a subset of γδ T cells committed to IL-17 production and are characterized by the expression of IL-23R and CCR6 and lack of CD27 expression. γδT17 cells are believed to arise within a narrow time window during prenatal thymic development. In agreement with this concept, we show in this study that adult recipient mice of (IL-23R reporter) bone marrow selectively lack IL-23R γδT17 cells. Despite their absence in secondary lymphoid tissues during homeostasis, γδT17 cells emerge in bone marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cream (Aldara). We demonstrate that IL-1ß and IL-23 together are able to promote the development of bona fide γδT17 cells from peripheral CD122 IL-23R γδ T cells, whereas CD122 γδ T cells fail to convert into γδT17 cells and remain stable IFN-γ producers (γδT1 cells). IL-23 is instrumental in expanding extrathymically generated γδT17 cells. In particular, TCR-Vγ4 chain-expressing CD122 IL-23R γδ T cells are induced to express IL-23R and IL-17 outside the thymus during skin inflammation. In contrast, TCR-Vγ1 γδ T cells largely resist this process because prior TCR engagement in the thymus has initiated their commitment to the γδT1 lineage. In summary, our data reveal that the peripheral pool of γδ T cells retains a considerable degree of plasticity because it harbors "naive" precursors, which can be induced to produce IL-17 and replenish peripheral niches that are usually occupied by thymus-derived γδT17 cells.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Psoríase/imunologia
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Aminoquinolinas
Animais
Diferenciação Celular
Células Cultivadas
Modelos Animais de Doenças
Seres Humanos
Interleucina-1beta/metabolismo
Subunidade beta de Receptor de Interleucina-2/metabolismo
Interleucina-23/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Receptores de Interleucina/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminoquinolines); 0 (Interleukin-17); 0 (Interleukin-1beta); 0 (Interleukin-2 Receptor beta Subunit); 0 (Interleukin-23); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-23 receptor, mouse); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700287


  8 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28835458
[Au] Autor:Corpuz TM; Vazquez-Lombardi R; Luong JK; Warren J; Stolp J; Christ D; King C; Brink R; Sprent J; Webster KE
[Ad] Endereço:Immunology Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia; and.
[Ti] Título:IL-2 Shapes the Survival and Plasticity of IL-17-Producing γδ T Cells.
[So] Source:J Immunol;199(7):2366-2376, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-17-producing γδ T (γδT-17) cells have proved to be an important early source of IL-17 in many inflammatory settings and are emerging as an important participant in protumor immune responses. Considering that their peripheral activation depends largely on innate signals rather than TCR ligation, it is important to understand what mechanisms exist to curb unwanted activation. Expression of the high-affinity IL-2R on γδT-17 cells prompted us to investigate a role for this cytokine. We found γδT-17 cells to be enriched, not depleted, in IL-2-deficient mice. The absence of IL-2 also resulted in higher IL-17 production and the emergence of IL-17 IFN-γ double producers. Furthermore, the addition of IL-2 to in vitro cultures of sorted γδT-17 cells was able to moderate IL-17 and affect differentiation into polyfunctional cytokine-producing cells. Interestingly, the Vγ6 subset was more susceptible to the effects of IL-2 than Vγ4 γδT-17 cells. We also found that unlike other γδ T cells, γδT-17 cells do not produce IL-2, but express Blimp-1, a known transcriptional repressor of IL-2. Although IL-2 was able to induce robust proliferation of γδT-17 cells, it did not sustain viability, negatively impacting their survival via downregulation of the IL-7R. Taken together, these data indicate that IL-2 can augment the γδT-17 response in favor of short-lived effectors with limited plasticity, particularly in the presence of IL-1ß and IL-23. In this way, IL-2 may act to curtail the innate-like response of γδT-17 cells upon arrival of IL-2-producing adaptive immune cells at the site of inflammation.
[Mh] Termos MeSH primário: Interleucina-17/biossíntese
Interleucina-2/imunologia
Interleucina-2/metabolismo
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Citocinas/biossíntese
Citometria de Fluxo
Inflamação
Interferon gama/biossíntese
Interferon gama/imunologia
Interleucina-17/imunologia
Interleucina-2/deficiência
Interleucina-2/genética
Interleucina-23/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Fator 1 de Ligação ao Domínio I Regulador Positivo
Receptores de Interleucina-7/genética
Transdução de Sinais
Linfócitos T/efeitos dos fármacos
Linfócitos T/fisiologia
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-17); 0 (Interleukin-2); 0 (Interleukin-23); 0 (Prdm1 protein, mouse); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin-7); 0 (Transcription Factors); 82115-62-6 (Interferon-gamma); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700335


  9 / 5792 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28798028
[Au] Autor:Wiede F; Dudakov JA; Lu KH; Dodd GT; Butt T; Godfrey DI; Strasser A; Boyd RL; Tiganis T
[Ad] Endereço:Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia Florian.Wiede@monash.edu.
[Ti] Título:PTPN2 regulates T cell lineage commitment and αß versus γδ specification.
[So] Source:J Exp Med;214(9):2733-2758, 2017 Sep 04.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the thymus, hematopoietic progenitors commit to the T cell lineage and undergo sequential differentiation to generate diverse T cell subsets, including major histocompatibility complex (MHC)-restricted αß T cell receptor (TCR) T cells and non-MHC-restricted γδ TCR T cells. The factors controlling precursor commitment and their subsequent maturation and specification into αß TCR versus γδ TCR T cells remain unclear. Here, we show that the tyrosine phosphatase PTPN2 attenuates STAT5 (signal transducer and activator of transcription 5) signaling to regulate T cell lineage commitment and SRC family kinase LCK and STAT5 signaling to regulate αß TCR versus γδ TCR T cell development. Our findings identify PTPN2 as an important regulator of critical checkpoints that dictate the commitment of multipotent precursors to the T cell lineage and their subsequent maturation into αß TCR or γδ TCR T cells.
[Mh] Termos MeSH primário: Linhagem da Célula/fisiologia
Proteína Tirosina Fosfatase não Receptora Tipo 2/fisiologia
Receptores de Antígenos de Linfócitos T alfa-beta/fisiologia
Receptores de Antígenos de Linfócitos T gama-delta/fisiologia
Linfócitos T/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células-Tronco Multipotentes/fisiologia
Fator de Transcrição STAT5/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (STAT5 Transcription Factor); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 2); EC 3.1.3.48 (Ptpn2 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161903


  10 / 5792 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28779024
[Au] Autor:Audemard-Verger A; Rivière M; Durand A; Peranzoni E; Guichard V; Hamon P; Bonilla N; Guilbert T; Boissonnas A; Auffray C; Eberl G; Lucas B; Martin B
[Ad] Endereço:Institut Cochin, CNRS UMR8104, INSERM U1016, Paris Descartes Université, 75014 Paris, France.
[Ti] Título:Macrophages Induce Long-Term Trapping of γδ T Cells with Innate-like Properties within Secondary Lymphoid Organs in the Steady State.
[So] Source:J Immunol;199(6):1998-2007, 2017 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:So far, peripheral T cells have mostly been described to circulate between blood, secondary lymphoid organs (SLOs), and lymph in the steady state. This nomadic existence would allow them to accomplish their surveying task for both foreign Ags and survival signals. Although it is now well established that γδ T cells can be rapidly recruited to inflammatory sites or in certain tumor microenvironments, the trafficking properties of peripheral γδ T cells have been poorly studied in the steady state. In the present study, we highlight the existence of resident γδ T cells in the SLOs of specific pathogen-free mice. Indeed, using several experimental approaches such as the injection of integrin-neutralizing Abs that inhibit the entry of circulating lymphocytes into lymph nodes and long-term parabiosis experiments, we have found that, contrary to Ly-6C CD44 and Ly-6C CD44 γδ T cells, a significant proportion of Ly-6C CD44 γδ T cells are trapped for long periods of time within lymph nodes and the spleen in the steady state. Specific in vivo cell depletion strategies have allowed us to demonstrate that macrophages are the main actors involved in this long-term retention of Ly-6C CD44 γδ T cells in SLOs.
[Mh] Termos MeSH primário: Linfonodos/imunologia
Macrófagos/imunologia
Baço/imunologia
Subpopulações de Linfócitos T/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/metabolismo
Comunicação Celular
Movimento Celular
Células Cultivadas
Receptores de Hialuronatos/metabolismo
Imunidade Inata
Vigilância Imunológica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Hyaluronan Receptors); 0 (Ly-6C antigen, mouse); 0 (Receptors, Antigen, T-Cell, gamma-delta)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700430



página 1 de 580 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