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  1 / 27211 MEDLINE  
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Aguiar, Maria Cássia Ferreira
Texto completo SciELO Brasil
[PMID]:29267664
[Au] Autor:Naufel AO; Aguiar MCF; Madeira FM; Abreu LG
[Ad] Endereço:Universidade Federal de Minas Gerais - UFMG, School of Dentistry, Department of Oral Surgery and Pathology, Belo Horizonte, MG, Brazil.
[Ti] Título:Treg and Th17 cells in inflammatory periapical disease: a systematic review.
[So] Source:Braz Oral Res;31:e103, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The process involved in periapical lesions, which occur as an outcome of pulpal necrosis, is regulated by the immune system including regulatory T cells (Treg) and T helper 17 cell (Th17) responses. The objective of this study was to conduct a frequency systematic review to determine the presence of Treg/Th17 responses and the influence of these cells in the progression of chronic inflammatory periapical lesions in humans. A systematic computerized search was carried out in Pubmed, Medline, Web of Science and Scopus electronic databases from their date of inception through the first week of May 2017. In addition, the reference lists of the included articles and the grey literature were hand-searched. Articles that evaluated the presence and influence of Treg/Th17 in the progression of human periapical lesions were included. Study selection and the quality assessment of the included articles (using the Newcastle-Ottawa scale) were carried out by two authors. Fifty-seven titles/abstracts were screened and eight studies met the eligibility criteria and were included in this systematic review. The included studies showed large variation in the type of periapical lesion assessed, mean age, age range, type of experiment and findings regarding the participation of Th17 and Treg in the status of inflammatory periapical lesions. The studies showed the involvement of Treg in the modulation of the inflammatory response in radicular cysts and periapical granulomas. This systematic review highlights the relationship between Treg and Th17 acting in a subtle balance inhibiting or promoting the progression of human periapical lesions.
[Mh] Termos MeSH primário: Periodontite Periapical/patologia
Linfócitos T Reguladores/patologia
Células Th17/patologia
[Mh] Termos MeSH secundário: Doença Crônica
Citocinas/análise
Progressão da Doença
Fatores de Transcrição Forkhead/análise
Seres Humanos
Periodontite Periapical/imunologia
Viés de Publicação
Linfócitos T Reguladores/imunologia
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


  2 / 27211 MEDLINE  
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[PMID]:29339767
[Au] Autor:Liu X; Mo W; Ye J; Li L; Zhang Y; Hsueh EC; Hoft DF; Peng G
[Ad] Endereço:Department of Internal Medicine, Division of Infectious Diseases, Allergy & Immunology, Saint Louis University School of Medicine, St Louis, MO, 63104, USA.
[Ti] Título:Regulatory T cells trigger effector T cell DNA damage and senescence caused by metabolic competition.
[So] Source:Nat Commun;9(1):249, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Defining the suppressive mechanisms used by regulatory T (Treg) cells is critical for the development of effective strategies for treating tumors and chronic infections. The molecular processes that occur in responder T cells that are suppressed by Treg cells are unclear. Here we show that human Treg cells initiate DNA damage in effector T cells caused by metabolic competition during cross-talk, resulting in senescence and functional changes that are molecularly distinct from anergy and exhaustion. ERK1/2 and p38 signaling cooperate with STAT1 and STAT3 to control Treg-induced effector T-cell senescence. Human Treg-induced T-cell senescence can be prevented via inhibition of the DNA damage response and/or STAT signaling in T-cell adoptive transfer mouse models. These studies identify molecular mechanisms of human Treg cell suppression and indicate that targeting Treg-induced T-cell senescence is a checkpoint for immunotherapy against cancer and other diseases associated with Treg cells.
[Mh] Termos MeSH primário: Dano ao DNA
Sistema de Sinalização das MAP Quinases
Linfócitos T Reguladores/fisiologia
[Mh] Termos MeSH secundário: Senescência Celular
Glucose/metabolismo
Seres Humanos
Imunoterapia
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT1/fisiologia
Fator de Transcrição STAT3/metabolismo
Fator de Transcrição STAT3/fisiologia
Linfócitos T Reguladores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02689-5


  3 / 27211 MEDLINE  
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[PMID]:29295981
[Au] Autor:Kimura K; Hohjoh H; Fukuoka M; Sato W; Oki S; Tomi C; Yamaguchi H; Kondo T; Takahashi R; Yamamura T
[Ad] Endereço:Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502, Japan.
[Ti] Título:Circulating exosomes suppress the induction of regulatory T cells via let-7i in multiple sclerosis.
[So] Source:Nat Commun;9(1):17, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Multiple sclerosis (MS) is a T cell-mediated autoimmune disease of the central nervous system. Foxp3 regulatory T (Treg) cells are reduced in frequency and dysfunctional in patients with MS, but the underlying mechanisms of this deficiency are unclear. Here, we show that induction of human IFN-γ IL-17A Foxp3 CD4 T cells is inhibited in the presence of circulating exosomes from patients with MS. The exosomal miRNA profile of patients with MS differs from that of healthy controls, and let-7i, which is markedly increased in patients with MS, suppresses induction of Treg cells by targeting insulin like growth factor 1 receptor (IGF1R) and transforming growth factor beta receptor 1 (TGFBR1). Consistently, the expression of IGF1R and TGFBR1 on circulating naive CD4 T cells is reduced in patients with MS. Thus, our study shows that exosomal let-7i regulates MS pathogenesis by blocking the IGF1R/TGFBR1 pathway.
[Mh] Termos MeSH primário: Exossomos/imunologia
MicroRNAs/imunologia
Esclerose Múltipla/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Adulto
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Exossomos/genética
Exossomos/metabolismo
Feminino
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Seres Humanos
Interleucina-17/genética
Interleucina-17/imunologia
Interleucina-17/metabolismo
Masculino
MicroRNAs/genética
Meia-Idade
Esclerose Múltipla/sangue
Esclerose Múltipla/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/imunologia
Proteínas Serina-Treonina Quinases/metabolismo
Receptores de Somatomedina/genética
Receptores de Somatomedina/imunologia
Receptores de Somatomedina/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/imunologia
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Linfócitos T Reguladores/metabolismo
Transcriptoma/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (IGF1R protein, human); 0 (IL17A protein, human); 0 (Interleukin-17); 0 (MicroRNAs); 0 (Receptors, Somatomedin); 0 (Receptors, Transforming Growth Factor beta); 0 (mirnlet7 microRNA, human); EC 2.7.1.11 (TGF-beta type I receptor); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02406-2


  4 / 27211 MEDLINE  
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[PMID]:28460478
[Au] Autor:Vo MC; Nguyen-Pham TN; Lee HJ; Jaya Lakshmi T; Yang S; Jung SH; Kim HJ; Lee JJ
[Ad] Endereço:Research Center for Cancer Immunotherapy, Chonnam National University Hwasun Hospital, Hwasun, Jeollanamdo, Republic of Korea.
[Ti] Título:Combination therapy with dendritic cells and lenalidomide is an effective approach to enhance antitumor immunity in a mouse colon cancer model.
[So] Source:Oncotarget;8(16):27252-27262, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we investigated efficacy of lenalidomide in combination with tumor antigen-loaded dendritic cells (DCs) in murine colon cancer model. MC-38 cell lines were injected subcutaneously to establish colon cancer-bearing mice. After tumor growth, lenalidomide (50 mg/kg/day) was injected intraperitoneally on 3 consecutive days in combination with tumor antigen-loaded DC vaccination on days 8, 12, 16, and 20. The tumor antigen-loaded DCs plus lenalidomide combination treatment exhibited a significant inhibition of tumor growth compared with the other groups. These effects were associated with a reduction in immune suppressor cells, such as myeloid-derived suppressor cells and regulatory T cells, with the induction of immune effector cells, such as natural killer cells, CD4+ T cells and CD8+ T cells in spleen, and with the activation of cytotoxic T lymphocytes and NK cells. This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response. This combination approach with DCs and lenalidomide may provide a new therapeutic option to improve the treatment of colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/imunologia
Neoplasias do Colo/patologia
Células Dendríticas/imunologia
Imunidade
Talidomida/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/imunologia
Vacinas Anticâncer/administração & dosagem
Vacinas Anticâncer/imunologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Neoplasias do Colo/genética
Neoplasias do Colo/terapia
Terapia Combinada
Citocinas/biossíntese
Células Dendríticas/metabolismo
Modelos Animais de Doenças
Feminino
Expressão Gênica
Imunidade/efeitos dos fármacos
Imunoterapia
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/metabolismo
Camundongos
Linfócitos T Citotóxicos/efeitos dos fármacos
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Talidomida/farmacologia
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Cancer Vaccines); 0 (Cytokines); 4Z8R6ORS6L (Thalidomide); F0P408N6V4 (lenalidomide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15917


  5 / 27211 MEDLINE  
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[PMID]:28453219
[Au] Autor:Worsham DN; Reems JA; Szczepiorkowski ZM; McKenna DH; Leemhuis T; Mathew AJ; Cancelas JA; Biomedical Excellence for Safer Transfusion (BEST) Collaborative Group
[Ad] Endereço:Hoxworth Blood Center, University of Cincinnati, Cincinnati, Ohio.
[Ti] Título:Clinical methods of cryopreservation for donor lymphocyte infusions vary in their ability to preserve functional T-cell subpopulations.
[So] Source:Transfusion;57(6):1555-1565, 2017 06.
[Is] ISSN:1537-2995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cryopreserved donor lymphocyte infusion (DLI) products are manufactured and administered to treat relapse after allogeneic hematopoietic stem cell transplantation. Reported clinical responses to DLIs vary broadly, even within the same group of patients. While there is an implicit recognition of the fact that different manufacturing protocols may have specific effects on different cell types, cryopreservation protocols are frequently derived from our experience in the cryopreservation of stem cell products and do not account for the heterogeneous functional nature of DLI T-cell populations. Here, we report the results of a prospective, multicenter trial on the effect of four different cryopreservation solutions that were used to freeze DLIs compared to control DLIs that were refrigerated overnight. STUDY DESIGN AND METHODS: Cryopreserved postthawed and refrigerated specimens were analyzed side by side for their T-cell subpopulation content and viability, as well as T-cell proliferation, cytokine secretion, and cytotoxic activities. RESULTS: This study indicates that "homemade" 10% dimethyl sulfoxide (DMSO) results in reduced viability of different CD4+ T-cell populations, including T-helper, T-cytotoxic, and T-regulatory populations, and a decrease in their proliferative and cytotoxic response to immunologically relevant stimuli, while the use of solutions containing 5% DMSO with intracellular-like cryoprotectant stabilizers maintains T-cell function at levels similar to refrigerated control samples. CONCLUSION: This study has important implications in determining the best cryoprotectant solution for specific clinical applications in allogeneic immunotherapy.
[Mh] Termos MeSH primário: Criopreservação/métodos
Transfusão de Linfócitos/métodos
[Mh] Termos MeSH secundário: Linfócitos T CD4-Positivos/citologia
Linfócitos T CD4-Positivos/imunologia
Ciclo Celular/fisiologia
Dimetil Sulfóxido/química
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Imunofenotipagem
Linfócitos T Citotóxicos/citologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Auxiliares-Indutores/citologia
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Reguladores/citologia
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1111/trf.14112


  6 / 27211 MEDLINE  
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[PMID]:28450656
[Au] Autor:Amin HZ; Sasaki N; Hirata KI
[Ad] Endereço:Department of Internal Medicine, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia. Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan. Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan. hilman_amin@yahoo.co.id.
[Ti] Título:Regulatory T Cell Immunity in Atherosclerosis.
[So] Source:Acta Med Indones;49(1):63-68, 2017 Jan.
[Is] ISSN:0125-9326
[Cp] País de publicação:Indonesia
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis is a chronic inflammatory disorder involving innate and adaptive immunity process. Effector T cell (Teff) responses promote atherosclerotic disease, whereas regulatory T cells (Tregs) have been shown to play a protective role against atherosclerosis by down-regulating inflammatory responses which include multiple mechanisms. Compelling experimental data suggest that shifting the Treg/Teff balance toward Tregs may be a possible therapeutic approach for atherosclerotic disease, although the role of Tregs in human atherosclerotic disease has not been fully elucidated. In this review, we discuss recent advances in our understanding of the roles of Tregs and Teffs in experimental atherosclerosis, as well as human coronary artery disease.
[Mh] Termos MeSH primário: Aterosclerose/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Inflamação/imunologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  7 / 27211 MEDLINE  
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[PMID]:29360858
[Au] Autor:Zhang A; Yang X; Li Q; Yang Y; Zhao G; Wang B; Wu D
[Ad] Endereço:Xinjiang Key Lab of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
[Ti] Título:Immunostimulatory activity of water-extractable polysaccharides from Cistanche deserticola as a plant adjuvant in vitro and in vivo.
[So] Source:PLoS One;13(1):e0191356, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A safe and effective vaccine adjuvant is important in modern vaccines. Various Chinese herbal polysaccharides can activate the immune system. Cistanche deserticola (CD) is a traditional Chinese herb and an adjuvant candidate. Here, we confirmed that water-extractable polysaccharides of CD (WPCD) could modulate immune responses in vitro and in vivo. In a dose-dependent manner, WPCD significantly promoted the maturation and function of murine marrow-derived dendritic cells (BM-DCs) through up-regulating the expression levels of MHC-II, CD86, CD80, and CD40, allogenic T cell proliferation, and the yields of IL-12 and TNF-α via toll-like receptor4 (TLR4), as indicated by in vitro experiments. In addition, its immunomodulatory activity was also observed in mice. WPCD effectively improved the titers of IgG, IgG1 and IgG2a and markedly enhanced the proliferation of T and B cells, the production of IFN-γ and IL-4 in CD4+ T cells and the expression level of IFN-γ in CD8+ T cells better than Alum. Furthermore, WPCD could markedly up-regulate the expression levels of CD40 and CD80 on DCs in spleen and down-regulate the Treg frequency. The study suggests that polysaccharides of Cistanche deserticola are a safe and effective vaccine adjuvant for eliciting both humoral immunity and cellular immunity by activating DCs via TLR4 signaling pathway.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Cistanche/química
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/administração & dosagem
Adjuvantes Imunológicos/isolamento & purificação
Animais
Diferenciação Celular/efeitos dos fármacos
Células Dendríticas/citologia
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Medicamentos de Ervas Chinesas/administração & dosagem
Medicamentos de Ervas Chinesas/farmacologia
Feminino
Imunidade Celular/efeitos dos fármacos
Imunidade Humoral/efeitos dos fármacos
Imunogenicidade da Vacina/efeitos dos fármacos
Técnicas In Vitro
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos ICR
Ovalbumina/administração & dosagem
Ovalbumina/imunologia
Plantas Medicinais/química
Polissacarídeos/administração & dosagem
Polissacarídeos/isolamento & purificação
Solubilidade
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Receptor 4 Toll-Like/metabolismo
Água
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Drugs, Chinese Herbal); 0 (Polysaccharides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 059QF0KO0R (Water); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191356


  8 / 27211 MEDLINE  
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[PMID]:29352298
[Au] Autor:Varanasi SK; Jaggi U; Hay N; Rouse BT
[Ad] Endereço:Department of Genome Science and Technology, University of Tennessee, Knoxville, Tennessee, United States of America.
[Ti] Título:Hexokinase II may be dispensable for CD4 T cell responses against a virus infection.
[So] Source:PLoS One;13(1):e0191533, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activation of CD4 T cells leads to their metabolic reprogramming which includes enhanced glycolysis, catalyzed through hexokinase enzymes. Studies in some systems indicate that the HK2 isoform is the most up regulated isoform in activated T cells and in this report the relevance of this finding is evaluated in an infectious disease model. Genetic ablation of HK2 was achieved in only T cells and the outcome was evaluated by measures of T cell function. Our results show that CD4 T cells from both HK2 depleted and WT animals displayed similar responses to in vitro stimulation and yielded similar levels of Th1, Treg or Th17 subsets when differentiated in vitro. A modest increase in the levels of proliferation was observed in CD4 T cells lacking HK2. Deletion of HK2 led to enhanced levels of HK1 indicative of a compensatory mechanism. Finally, CD4 T cell mediated immuno-inflammatory responses to a virus infection were similar between WT and HK2 KO animals. The observations that the expression of HK2 appears non-essential for CD4 T cell responses against virus infections is of interest since it suggests that targeting HK2 for cancer therapy may not have untoward effects on CD4 T cell mediated immune response against virus infections.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/enzimologia
Linfócitos T CD4-Positivos/imunologia
Hexoquinase/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/patologia
Diferenciação Celular/imunologia
Modelos Animais de Doenças
Feminino
Herpesvirus Humano 1
Hexoquinase/deficiência
Hexoquinase/genética
Ceratite Herpética/enzimologia
Ceratite Herpética/imunologia
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Linfócitos T Reguladores/imunologia
Células Th1/imunologia
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 2.7.1.1 (Hexokinase); EC 2.7.1.1 (hexokinase 2, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191533


  9 / 27211 MEDLINE  
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[PMID]:29327244
[Au] Autor:Menssen HD; Harnack U; Erben U; Neri D; Hirsch B; Dürkop H
[Ad] Endereço:Division of Hematology and Oncology, Campus Benjamin Franklin, Department of Medicine, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany. hans_dietrich.menssen@charite.de.
[Ti] Título:Antibody-based delivery of tumor necrosis factor (L19-TNFα) and interleukin-2 (L19-IL2) to tumor-associated blood vessels has potent immunological and anticancer activity in the syngeneic J558L BALB/c myeloma model.
[So] Source:J Cancer Res Clin Oncol;144(3):499-507, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To analyze the impact of TNFα or IL2 on human lymphocytes in vitro and the anti-tumor and immune-modifying effects of L19-IL2 and L19-TNFα on subcutaneously growing J558L myeloma in immunocompetent mice. METHODS: PBMCs from three healthy volunteers were incubated with IL2, TNFα, or with IL2 plus addition of TNFα (final 20 h). BALB/c J558L mice with subcutaneous tumors were treated with intravenous L19-TNFα plus L19-IL2, or controls. Tumor growth and intra- and peri-tumoral tissues were analyzed for micro-vessel density, necrosis, immune cell composition, and PD1 or PD-L1 expressing cells. RESULTS: Exposure of PBMC in vitro to IL2, TNFα, or to IL2 over 3 and 5 days plus TNFα for the final 20 h resulted in an approximately 50 and 75% reduction of the CD25low effector cell/CD25high Treg cell ratio, respectively, compared to medium control. IL2 or TNFα increased the proportion of CD4- CD25low effector lymphocytes while reducing the proportion of CD4+ CD25low Teff cells. In the J558L myeloma model, tumor eradication was observed in 58, 42, 25, and 0% of mice treated with L19-TNFα plus L19-IL2, L19-TNFα, L19-IL2, and PBS, respectively. L19-TNFα/L19-IL2 combination caused tumor necrosis, capillary density doubling, peri-tumoral T cell and PD1+ T cell reduction (- 50%), and an increase in PD-L1+ myeloma cells. CONCLUSION: IL2, TNFα, or IL2 plus TNFα (final 20 h) increased the proportion of CD4- CD25low effector lymphocytes possibly indicating immune activation. L19-TNFα/L19-IL2 combination therapy eradicated tumors in J558L myeloma BALB/c mice likely via TNFα-induced tumor necrosis and L19-TNFα/L19-IL2-mediated local cellular immune reactions.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/uso terapêutico
Anticorpos Monoclonais/uso terapêutico
Imunoterapia/métodos
Interleucina-2/uso terapêutico
Mieloma Múltiplo/terapia
Neovascularização Patológica/tratamento farmacológico
Fator de Necrose Tumoral alfa/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Vacinas Anticâncer/uso terapêutico
Linhagem Celular Tumoral
Sistemas de Liberação de Medicamentos
Feminino
Imunotoxinas/uso terapêutico
Camundongos
Camundongos Endogâmicos BALB C
Mieloma Múltiplo/imunologia
Mieloma Múltiplo/patologia
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Transplante Isogênico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Antibodies, Monoclonal); 0 (Cancer Vaccines); 0 (Immunotoxins); 0 (Interleukin-2); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2564-6


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[PMID]:29293622
[Au] Autor:Ma Y; Dawicki W; Zhang X; Gordon JR
[Ad] Endereço:Division of Respirology, Critical Care and Sleep Medicine, Department of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
[Ti] Título:Contributions of direct versus indirect mechanisms for regulatory dendritic cell suppression of asthmatic allergen-specific IgG1 antibody responses.
[So] Source:PLoS One;13(1):e0190414, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-10-differentiated dendritic cells (DC10) can reverse the asthma phenotype in mice, but how they suppress the asthmatic B cell response is unclear. Herein we assessed the mechanism(s) by which DC10 and DC10-induced Treg affect IgG1 production in asthma. We observed a rapid decline in lung-resident OVA-specific IgG1-secreting B cells on cessation of airway allergen challenge, and intraperitoneal DC10 therapy did not amplify that (p>0.05). It did however increase the loss of IgG1-B cells from the bone marrow (by 45+/-7.2%; p≤0.01) and spleen (by 65+/-17.8%; p≤0.05) over 2 wk. Delivery of OVA-loaded DC10 directly into the airways of asthmatic mice decreased the lung IgG1 B cell response assessed 2 dy later by 33+/-9.7% (p≤0.01), while their co-culture with asthmatic lung cell suspensions reduced the numbers of IgG1-secreting cells by 56.5+/-9.7% (p≤0.01). This effect was dependent on the DC10 carrying intact allergen on their cell surface; DC10 that had phagocytosed and fully processed their allergen were unable to suppress B cell responses, although they did suppress asthmatic Th2 cell responses. We had shown that therapeutic delivery of DC10-induced Treg can effectively suppress asthmatic T and B cell (IgE and IgG1) responses; herein CD4+ cells or Treg from the lungs of DC10-treated OVA-asthmatic mice suppressed in vitro B cell IgG1 production by 52.2+/-8.7% (p≤0.001) or 44.6+/-12.2% (p≤0.05), respectively, but delivery of DC10-induced Treg directly into the airways of asthmatic mice had no discernible impact over 2 dy on the numbers of lung IgG1-secreting cells (p≥0.05). In summary, DC10 treatment down-regulates OVA-specific B cell responses of asthmatic mice. While DC10 that carry intact allergen on their cell surface can dampen this response, DC10-induced Treg are critical for full realization of this outcome. This suggests that infectious tolerance is an essential element in regulatory DC control of the B cell response in allergic asthma.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Asma/imunologia
Imunoglobulina G/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Separação Celular
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Camundongos
Camundongos Endogâmicos BALB C
Ovalbumina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Allergens); 0 (Immunoglobulin G); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190414



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