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[PMID]:25925868
[Au] Autor:Janelle V; Carli C; Taillefer J; Orio J; Delisle JS
[Ad] Endereço:Centre de recherche de l'Hôpital Maisonneuve-Rosemont, Montreal, Quebec, Canada. vjanelle@pcitp.org.
[Ti] Título:Defining novel parameters for the optimal priming and expansion of minor histocompatibility antigen-specific T cells in culture.
[So] Source:J Transl Med;13:123, 2015 Apr 19.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Adoptive transfer of minor histocompatibility antigen (MiHA)-specific T cells is a promising therapy for patients with hematological cancers. However, the efficacy of the transferred cells is hampered by the acquisition of terminal effector differentiation and exhaustion features during expansion in vitro thus preventing their function and persistence in vivo. Yet, the factors that induce T-cell differentiation and functional impairment in culture remain poorly defined and are likely to vary depending on the method used for expansion. METHODS: Using the clinically relevant HLA-A0201-restricted MiHA HA-1 as well as reagents and procedures that are readily transferable to a clinical environment, we designed a novel culture protocol and defined how exhaustion features appeared in function of time. The optimal time points for the expansion of "fit" MiHA-specific T cells were delineated using phenotypic and functional assessments including KLRG-1 and PD-1 surface markers as well as Ki67 staining and cytokine secretion assays. RESULTS: Following a priming phase, an enrichment step and a rapid expansion stage, our method generates MiHA-specific T-cell lines. Evidence of phenotypic and functional dysfunction appear in function of culture duration, but display different characteristics following the extension of the priming or rapid expansion phases. While repeated antigen exposure during the priming phase induced the decline of the antigen-specific population and the expression of PD-1 and KLRG-1 on antigen-specific CD8+ T cells, the prolongation of an antigen-free expansion phase induced proliferation arrest and the relative loss of antigen-specific cells without impairing polyfunctional cytokine secretion or inducing PD-1 and KLRG-1 expression. A similar pattern was also observed after stimulating a virus-specific memory repertoire, except for the more rapid acquisition of exhaustion features upon repeated antigen exposure. CONCLUSION: Our results offer novel insights on the impact of culture duration on the acquisition of T-cell exhaustion features. Using a new clinical-compliant protocol, we define critical parameters to monitor in order to optimally differentiate and expand MiHA-specific T cells in culture prior to adoptive transfer.
[Mh] Termos MeSH primário: Antígenos Secundários de Estimulação de Linfócitos/imunologia
Linfócitos T/citologia
[Mh] Termos MeSH secundário: Reatores Biológicos
Linhagem Celular
Proliferação Celular
Técnicas de Cocultura
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Imunoterapia Adotiva
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Minor Lymphocyte Stimulatory Antigens)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150501
[St] Status:MEDLINE
[do] DOI:10.1186/s12967-015-0495-z


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[PMID]:25817463
[Au] Autor:Shima T; Inada K; Nakashima A; Ushijima A; Ito M; Yoshino O; Saito S
[Ad] Endereço:Department of Obstetrics and Gynecology, University of Toyama, Toyama 930-0194, Japan.
[Ti] Título:Paternal antigen-specific proliferating regulatory T cells are increased in uterine-draining lymph nodes just before implantation and in pregnant uterus just after implantation by seminal plasma-priming in allogeneic mouse pregnancy.
[So] Source:J Reprod Immunol;108:72-82, 2015 Apr.
[Is] ISSN:1872-7603
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Paternal antigen-specific regulatory T (PA-specific Treg) cells play an important role in feto-maternal tolerance. To detect the PA-specific Tregs, female BALB/c mice were mated with male DBA/2 mice. Mls Ia antigen on DBA/2 mice is recognized by the T-cell receptor Vß6; thus, CD4(+)Foxp3(+)Vß6(+) cells are recognized as PA-specific Treg cells. CD4(+)CD25(+)Vß6(+) cells effectively suppressed the allo-reactive proliferation of lymphocytes compared with that of CD4(+)CD25(+)Vß6(-) cells. Vß6(+) PA-specific Treg cells expressed CCR4 and CCR5 on their surface. The frequency of Ki67(+) PA-specific Treg cells among Treg cells was significantly increased in draining lymph nodes on day 3.5 post-coitus (pc; 6.8±1.1%, p<0.05) and day 5.5 pc (7.2±1.1%, p<0.05) in allogeneic pregnant mice compared with that in nonpregnant mice (2.7±0.2%). The frequency of Ki67(+) PA-specific Treg cells in the uterus increased significantly after day 5.5 pc in allogeneic pregnant mice compared with that in nonpregnant mice (8.8±2.8% vs. 1.2±1.3%, p<0.05). However, Ki67(-)PA-specific Tregs did not change during pregnancy. To analyze the role of seminal fluid or sperm in Treg expansion, female BALB/c mice were mated with vasectomized DBA/2 male mice (VAS) or seminal vesicle-excised DBA/2 male mice (SVX). The frequency of Ki67(+) PA-specific Treg cells did not increase in draining lymph nodes or uterus in BALB/c×DBA/2 (SVX) allogeneic mating mice. These findings suggest that the priming by seminal fluid is important for the induction of proliferating PA-specific Tregs in uterine-draining lymph nodes just before implantation and pregnant uterus after implantation, resulting in successful implantation and the maintenance of allogeneic pregnancy.
[Mh] Termos MeSH primário: Implantação do Embrião/imunologia
Linfonodos/imunologia
Sêmen/imunologia
Linfócitos T Reguladores/imunologia
Útero/imunologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Células Cultivadas
Feminino
Fatores de Transcrição Forkhead/metabolismo
Isoantígenos/imunologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos DBA
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Pais
Gravidez
Receptores de Antígenos de Linfócitos T alfa-beta/metabolismo
Receptores CCR4/metabolismo
Receptores CCR5/metabolismo
Vasectomia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCR5 protein, mouse); 0 (Ccr4 protein, mouse); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Isoantigens); 0 (Minor Lymphocyte Stimulatory Antigens); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Receptors, CCR4); 0 (Receptors, CCR5)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150408
[Lr] Data última revisão:
150408
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150331
[St] Status:MEDLINE


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[PMID]:20127675
[Au] Autor:Ohkusu-Tsukada K; Toda M; Udono H; Kawakami Y; Takahashi K
[Ad] Endereço:Department of Veterinary Pathology, Nippon Veterinary and Life-science University (NVLU), Tokyo, Japan. tkd-oks@nvlu.ac.jp
[Ti] Título:Targeted inhibition of IL-10-secreting CD25- Treg via p38 MAPK suppression in cancer immunotherapy.
[So] Source:Eur J Immunol;40(4):1011-21, 2010 Apr.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Cancer-induced immunotolerance mediated by inducible Treg (iTreg) is a major obstacle to cancer immunotherapy. In a basic study of immunotolerance, injection of an endogenous superantigen, i.e. the minor lymphocyte stimulatory (Mls)-1(a), into specific TCR Vbeta8.1-Tg mice enabled generation of anergic CD25(-) iTreg, the immunosuppressive function of which was maintained by IL-10 production via p38-MAPK activation. Interestingly, although p38-chemical inhibitor (p38-inhibitor) is capable of breaking CD25(-) iTreg-induced immunotolerance, the p38-inhibitor had hardly any immunotolerance breaking effect when CD25(+) Treg were present, suggesting that depletion of CD25(+) Treg is necessary for p38-inhibitor to be effective. Peptide OVA(323-339) iv.-injection into its specific TCR-Tg (OT-II) mice also induced adaptive tolerance by iTreg. Peptide immunotherapy with p38-inhibitor after CD25(+) Treg-depletion was performed in an OVA-expressing lymphoma E.G7-bearing tolerant model established by adoptive transfer of OT-II CD25(-) iTreg, which resulted in suppression of tumor growth. Similarly, the antitumor immunity induced by peptide immunotherapy in colon carcinoma CT26-bearing mice, in which the number of IL-10-secreting iTreg is increased, was augmented by treatment with p38-inhibitor after CD25(+) Treg-depletion and resulted in inhibition of tumor progression. These results suggest that simultaneous inhibition of two distinct Treg-functions may be important to the success of cancer immunotherapy.
[Mh] Termos MeSH primário: Imidazóis/uso terapêutico
Imunoterapia Adotiva
Imunoterapia/métodos
Interleucina-10/secreção
Depleção Linfocítica/métodos
Linfoma não Hodgkin/terapia
Proteínas de Neoplasias/antagonistas & inibidores
Piridinas/uso terapêutico
Linfócitos T Reguladores/efeitos dos fármacos
Evasão Tumoral/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/biossíntese
Proteínas Adaptadoras de Transdução de Sinal/genética
Sequência de Aminoácidos
Animais
Anergia Clonal
Fatores de Transcrição Forkhead/biossíntese
Fatores de Transcrição Forkhead/genética
Imidazóis/farmacologia
Interleucina-10/biossíntese
Interleucina-10/genética
Subunidade alfa de Receptor de Interleucina-2/análise
Linfoma não Hodgkin/imunologia
Camundongos
Camundongos Endogâmicos
Camundongos Transgênicos
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Dados de Sequência Molecular
Proteínas de Neoplasias/fisiologia
Ovalbumina/imunologia
Fragmentos de Peptídeos/imunologia
Piridinas/farmacologia
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Superantígenos/imunologia
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/secreção
Receptor Toll-Like 9/biossíntese
Receptor Toll-Like 9/genética
Evasão Tumoral/imunologia
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Il2ra protein, mouse); 0 (Imidazoles); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Minor Lymphocyte Stimulatory Antigens); 0 (Neoplasm Proteins); 0 (OVA 323-339); 0 (Peptide Fragments); 0 (Pyridines); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Superantigens); 0 (Tab1 protein, mouse); 0 (Tlr9 protein, mouse); 0 (Toll-Like Receptor 9); 130068-27-8 (Interleukin-10); 9006-59-1 (Ovalbumin); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1005
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100204
[St] Status:MEDLINE
[do] DOI:10.1002/eji.200939513


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[PMID]:20072134
[Au] Autor:Varga G; Nippe N; Balkow S; Peters T; Wild MK; Seeliger S; Beissert S; Krummen M; Roth J; Sunderkötter C; Grabbe S
[Ad] Endereço:Department of Dermatology, University of Muenster, Muenster, Germany. varga@uni-muenster.de
[Ti] Título:LFA-1 contributes to signal I of T-cell activation and to the production of T(h)1 cytokines.
[So] Source:J Invest Dermatol;130(4):1005-12, 2010 Apr.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The beta(2) integrins are important for both transendothelial migration of leukocytes and T-cell activation during antigen presentation. In T cells, triggering of leukocyte functional antigen-1 (LFA-1) is required for full activation and T-helper (Th)1/Th2 differentiation. We used CD18-deficient (CD18(-/-)) mice to examine the role of LFA-1 in the activation of T cells. Compared with wild-type controls, CD18(-/-) T cells proliferated normally when stimulated with antibodies against CD3 and CD28, but secreted significantly less IFN-gamma and IL-2 than their wild-type counterparts. However, when T cells were stimulated with dendritic cells (DCs) that provide additional LFA-1 ligation, the proliferation of CD18(-/-) T cells was significantly reduced, whereas cytokine production remained impaired. The diminished proliferative capacity of CD18(-/-) T cells could be fully compensated for by additional triggering of the T-cell receptor, but not by additional stimulation through the costimulatory molecule, CD28. Thus, ligation of LFA-1 on T cells participates in regulation of Th1 cytokines in vivo. In addition, LFA-1 primarily exerts an effect as an enhancer of TCR signalling and does not facilitate classical costimulation.
[Mh] Termos MeSH primário: Interferon gama/metabolismo
Interleucina-2/metabolismo
Antígeno-1 Associado à Função Linfocitária/metabolismo
Antígenos Secundários de Estimulação de Linfócitos/fisiologia
Células Th1/citologia
Células Th1/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos/farmacologia
Antígenos CD18/genética
Antígenos CD18/metabolismo
Antígenos CD28/imunologia
Complexo CD3/imunologia
Adesão Celular/imunologia
Diferenciação Celular/imunologia
Divisão Celular/imunologia
Células Dendríticas/citologia
Células Dendríticas/imunologia
Molécula 1 de Adesão Intercelular/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Transdução de Sinais/imunologia
Células Th1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies); 0 (CD18 Antigens); 0 (CD28 Antigens); 0 (CD3 Complex); 0 (Interleukin-2); 0 (Lymphocyte Function-Associated Antigen-1); 0 (Minor Lymphocyte Stimulatory Antigens); 126547-89-5 (Intercellular Adhesion Molecule-1); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1004
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100115
[St] Status:MEDLINE
[do] DOI:10.1038/jid.2009.398


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[PMID]:19249120
[Au] Autor:Silberman D; Bucknum A; Kozlowski M; Matlack R; Riggs J
[Ad] Endereço:Department of Biology, Rider University, Lawrenceville, NJ 08648-3099, USA.
[Ti] Título:Cytokine treatment of macrophage suppression of T cell activation.
[So] Source:Immunobiology;215(1):70-80, 2010.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:High Mphi:T cell ratios suppress the immune response to the retroviral superantigen Mls by IFNgamma-triggered production of the arg- and trp-consuming enzymes iNOS and IDO. Attempts to reverse suppression by treatment with pro-inflammatory cytokines revealed that IL-6 improved the T cell response to Mls and the pro-hematopoietic cyokines IL-3 and GM-CSF increased suppression. GM-CSF treatment increased Mphi expression of CD80, a ligand for the immune suppressive B7H1 and CTLA-4 receptors. These results illustrate potential strategies for reversing the suppression of cell-mediated immunity characteristic of the high Mphi:T cell ratios found in many tumors.
[Mh] Termos MeSH primário: Citocinas/biossíntese
Tolerância Imunológica/efeitos dos fármacos
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo
Ativação Linfocitária/imunologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Neoplasias/imunologia
Óxido Nítrico Sintase Tipo II/metabolismo
Linfócitos T/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos CD/metabolismo
Antígeno B7-1/genética
Antígeno B7-1/imunologia
Antígeno B7-1/metabolismo
Antígeno CTLA-4
Comunicação Celular/efeitos dos fármacos
Comunicação Celular/imunologia
Células Cultivadas
Citocinas/genética
Citocinas/imunologia
Citocinas/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Imunoterapia
Indolamina-Pirrol 2,3,-Dioxigenase/genética
Indolamina-Pirrol 2,3,-Dioxigenase/imunologia
Interferon gama/biossíntese
Interferon gama/genética
Interferon gama/secreção
Ativação Linfocitária/efeitos dos fármacos
Macrófagos/metabolismo
Macrófagos/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos SCID
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Neoplasias/metabolismo
Neoplasias/patologia
Neoplasias/terapia
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/imunologia
Linfócitos T/imunologia
Linfócitos T/metabolismo
Linfócitos T/patologia
Evasão Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (B7-1 Antigen); 0 (CTLA-4 Antigen); 0 (Ctla4 protein, mouse); 0 (Cytokines); 0 (Indoleamine-Pyrrole 2,3,-Dioxygenase); 0 (Minor Lymphocyte Stimulatory Antigens); 82115-62-6 (Interferon-gamma); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1005
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090303
[St] Status:MEDLINE
[do] DOI:10.1016/j.imbio.2009.01.015


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[PMID]:19657087
[Au] Autor:Tanriver Y; Martín-Fontecha A; Ratnasothy K; Lombardi G; Lechler R
[Ad] Endereço:Medical Research Council Centre for Transplantation, King's College London, School of Medicine, Guy's Hospital, London, United Kingdom.
[Ti] Título:Superantigen-activated regulatory T cells inhibit the migration of innate immune cells and the differentiation of naive T cells.
[So] Source:J Immunol;183(5):2946-56, 2009 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulatory T cells can be used as tools to suppress pathogenic T cells in autoimmunity, graft-vs-host-disease, and transplantation. But even when high numbers of Ag-specific regulatory T cells are available, it is still possible under certain in vivo and in vitro conditions for effector T cells to escape effective control. Current reports suggest that the degree of suppression is modulated by the inflammatory milieu, which can induce resistance to suppression in effector T cells or subvert the inhibitory function of the regulatory T cells. Cells of the innate immune system integrate early signals of injury and infection and have a major impact on the ensuing inflammation. Hence, the modification of these initial events can be key to allowing suppression to dominate. The approach we took here was to test whether the in vivo preactivation of endogenous regulatory T cells with a superantigen could enhance their suppressive potency. We provide evidence that this not only proved effective in expanding the pool of preactivated regulatory T cells but also in preventing the migration of NK cells and granulocytes upon sensitization with matured dendritic cells. The attenuation of innate immune activation was accompanied by linked suppression of adoptively transferred OVA-specific T cells when APC coexpressing OVA and the superantigen were injected. These data suggest that the preactivation of regulatory T cells is a promising approach to increase their potency.
[Mh] Termos MeSH primário: Diferenciação Celular/imunologia
Inibição de Migração Celular/imunologia
Imunidade Inata
Ativação Linfocitária/imunologia
Fase de Repouso do Ciclo Celular/imunologia
Superantígenos/fisiologia
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Fatores de Transcrição Forkhead/biossíntese
Depleção Linfocítica
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos DBA
Camundongos Transgênicos
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Baço/citologia
Baço/imunologia
Baço/transplante
Subpopulações de Linfócitos T/citologia
Subpopulações de Linfócitos T/metabolismo
Linfócitos T Reguladores/metabolismo
Linfócitos T Reguladores/transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Minor Lymphocyte Stimulatory Antigens); 0 (Superantigens)
[Em] Mês de entrada:0909
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:090807
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.0803953


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[PMID]:15638126
[Au] Autor:Rosini L; Matlack R; Taylor J; Howell KF; Yeh K; Pennello A; Riggs JE
[Ad] Endereço:Department of Biology, Rider University, Lawrenceville, NJ 08648-3099, USA.
[Ti] Título:Nonlymphoid peritoneal cells suppress the T cell response to Mls.
[So] Source:Immunobiology;209(8):575-84, 2004.
[Is] ISSN:0171-2985
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Comparative analyses of the ability of lymphoid tissue to present the minor lymphocyte stimulatory (Mls) superantigen Mls-1a in vitro revealed that all tissues containing mature B cells, except peritoneal cavity (PerC) cells, induced Mls-1a-specific T cell activation. Irradiation and mitomycin C treatment, addition of IL-2 and IL-12, and neutralization of IL-10 and TGF-beta did not restore Mls-1a antigen presentation by PerC cells. Co-culture studies revealed that PerC cells actively suppress the T cell response to Mls-1a. PerC cells from severe-combined immune-defective (SCID) mice also suppressed this response indicating that nonlymphoid cells mediate this effect. These results suggest that in addition to antigen processing and presentation, resident peritoneal cavity cells may temper lymphocyte activation.
[Mh] Termos MeSH primário: Células Apresentadoras de Antígenos/imunologia
Tolerância Imunológica
Ativação Linfocitária/imunologia
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Cavidade Peritoneal/citologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/imunologia
Células Apresentadoras de Antígenos/efeitos dos fármacos
Células Apresentadoras de Antígenos/efeitos da radiação
Apoptose
Linfócitos B/imunologia
Comunicação Celular/imunologia
Técnicas de Cocultura
Citocinas/imunologia
Citocinas/farmacologia
Citocinas/fisiologia
Feminino
Tecido Linfoide/citologia
Tecido Linfoide/imunologia
Masculino
Camundongos
Camundongos Endogâmicos
Camundongos Mutantes
Mitomicina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Cytokines); 0 (Minor Lymphocyte Stimulatory Antigens); 50SG953SK6 (Mitomycin)
[Em] Mês de entrada:0504
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050111
[St] Status:MEDLINE


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[PMID]:15518337
[Au] Autor:Riggs JE; Howell KF; Taylor J; Mahjied T; Prokopenko N; Alvarez J; Coleman C
[Ad] Endereço:Department of Biology, Rider University, 2083 Lawrenceville Road, Lawrenceville, NJ 08648-3099, USA. riggs@rider.edu
[Ti] Título:Mls presentation by peritoneal cavity B cells.
[So] Source:Immunobiology;209(3):255-64, 2004.
[Is] ISSN:0171-2985
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:DBA/2J spleen and peritoneal cells were compared for their ability to present the minor lymphocyte stimulatory superantigen Mls-1a. Although capable of Mls presentation in vivo, peritoneal cells were less effective than spleen cells in vitro. This difference was not due to cell concentration or culture duration. Flow cytometric comparison of spleen and peritoneal B cells revealed no significant differences in cell surface markers needed for cognate interaction with T cells. Resolution of peritoneal B cell subsets by cell sorting revealed that even though B-1 cells were capable of Mls presentation, they were less effective than B-2 cells. Mixing experiments showed that B-1 cells did not inhibit B-2 cell presentation of Mls. In contrast, total peritoneal cells inhibited T cell responses to Mls presented by spleen cells. The peritoneal cavity harbors B cells that can present Mls as well as other cells that can suppress this response.
[Mh] Termos MeSH primário: Apresentação do Antígeno/imunologia
Linfócitos B/imunologia
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Cavidade Peritoneal/citologia
[Mh] Termos MeSH secundário: Animais
Feminino
Masculino
Camundongos
Camundongos Endogâmicos
Antígenos Secundários de Estimulação de Linfócitos/metabolismo
Baço/citologia
Baço/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Minor Lymphocyte Stimulatory Antigens)
[Em] Mês de entrada:0502
[Cu] Atualização por classe:071114
[Lr] Data última revisão:
071114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:041103
[St] Status:MEDLINE


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[PMID]:15282297
[Au] Autor:Ohkusu-Tsukada K; Tominaga N; Udono H; Yui K
[Ad] Endereço:Division of Immunology, Department of Translational Medical Sciences, Graduate School of Biomedical Sciences, Nagasaki University, Sakamoto, Nagasaki, Japan.
[Ti] Título:Regulation of the maintenance of peripheral T-cell anergy by TAB1-mediated p38 alpha activation.
[So] Source:Mol Cell Biol;24(16):6957-66, 2004 Aug.
[Is] ISSN:0270-7306
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In anergic T cells, T-cell receptor (TCR)-mediated responses are functionally inactivated by negative regulatory signals whose mechanisms are poorly understood. Here, we show that CD4(+) T cells anergized in vivo by superantigen Mls-1(a) express a scaffolding protein, transforming growth factor beta-activated protein kinase 1-binding protein 1 (TAB1), that negatively regulates TCR signaling through the activation of mitogen-activated protein kinase p38 alpha. TAB1 was not expressed in naive and activated CD4(+) T cells. Inhibition of p38 activity in anergic T cells by a chemical inhibitor resulted in the recovery of interleukin 2 (IL-2) and the inhibition of IL-10 secretion. T-cell hybridoma 2B4 cells transduced with TAB1-containing retrovirus (TAB1-2B4 cells) showed activated p38 alpha, inhibited extracellular signal-regulated kinase (ERK) activity, culminating in reduced IL-2 levels and increased IL-10 production. The use of a p38 inhibitor or cotransfection of a dominant-negative form of p38 in TAB1-2B4 cells resulted in the recovery of ERK activity and IL-2 production. These results imply that TAB1-mediated activation of p38 alpha in anergic T cells regulates the maintenance of T-cell unresponsiveness both by inhibiting IL-2 production and by promoting IL-10 production.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal
Linfócitos T CD4-Positivos/fisiologia
Proteínas de Transporte/imunologia
Anergia Clonal
Peptídeos e Proteínas de Sinalização Intracelular
Proteínas Quinases Ativadas por Mitógeno/imunologia
Receptores de Antígenos de Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/citologia
Proteínas de Transporte/genética
Células Cultivadas
Ativação Enzimática
Inibidores Enzimáticos/metabolismo
Seres Humanos
Interleucina-10/imunologia
Interleucina-2/imunologia
Ativação Linfocitária
Sistema de Sinalização das MAP Quinases/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos CBA
Camundongos Transgênicos
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Proteínas Quinases Ativadas por Mitógeno/genética
Ratos
Receptores de Antígenos de Linfócitos T/genética
Transdução Genética
Proteínas Quinases p38 Ativadas por Mitógeno
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RETRACTED PUBLICATION
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Carrier Proteins); 0 (Enzyme Inhibitors); 0 (Interleukin-2); 0 (Intracellular Signaling Peptides and Proteins); 0 (Minor Lymphocyte Stimulatory Antigens); 0 (Receptors, Antigen, T-Cell); 0 (TAB1 protein, MAPKKK activator, vertebrate); 0 (TAB1 protein, human); 130068-27-8 (Interleukin-10); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:0409
[Cu] Atualização por classe:140608
[Lr] Data última revisão:
140608
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040730
[St] Status:MEDLINE


  10 / 323 MEDLINE  
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[PMID]:15219458
[Au] Autor:Bjursten M; Hultgren OH; Hultgren Hörnquist E
[Ad] Endereço:Department of Clinical Immunology, Göteborg University, S-413 46, Gothenburg, Sweden. malin.bjursten@microbio.gu.se
[Ti] Título:Enhanced pro-inflammatory cytokine production in Galphai2-deficient mice on colitis prone and colitis resistant 129Sv genetic backgrounds.
[So] Source:Cell Immunol;228(2):77-80, 2004 Apr.
[Is] ISSN:0008-8749
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mice deficient in G-protein subunit alphai2 develop colitis closely resembling human ulcerative colitis when raised on 129SvEv background. When backcrossing the Galphai2-deficiency into a 129SvJBom genetic background, surprisingly, mice did not develop colitis. In vitro stimulation of splenocytes with formalin-killed Staphylococcus aureus resulted in significantly increased production of interleukin-1beta, tumor necrosis factor, and interleukin-12p40 in Galphai2(-/-) as compared to control mice. The enhanced production of pro-inflammatory cytokines was seen in colitis prone as well as in colitis resistant genetic background. A similar outcome was seen upon stimulation with toxic shock syndrome toxin-1, a T cell superantigen, except that Galphai2(-/-) colitis resistant 129SvJBom splenocytes did not show increased production of IL-12p40 as compared to their controls.
[Mh] Termos MeSH primário: Colite/imunologia
Citocinas/biossíntese
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/deficiência
[Mh] Termos MeSH secundário: Animais
Toxinas Bacterianas/imunologia
Colite/genética
Colite/metabolismo
Citocinas/imunologia
Enterotoxinas/imunologia
Feminino
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/imunologia
Interleucina-1/biossíntese
Interleucina-1/imunologia
Interleucina-10/biossíntese
Interleucina-10/imunologia
Interleucina-12/biossíntese
Interleucina-12/imunologia
Subunidade p40 da Interleucina-12
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Antígenos Secundários de Estimulação de Linfócitos/imunologia
Subunidades Proteicas/biossíntese
Subunidades Proteicas/imunologia
Staphylococcus aureus/imunologia
Estatísticas não Paramétricas
Superantígenos/imunologia
Fator de Necrose Tumoral alfa/biossíntese
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Toxins); 0 (Cytokines); 0 (Enterotoxins); 0 (Interleukin-1); 0 (Interleukin-12 Subunit p40); 0 (Minor Lymphocyte Stimulatory Antigens); 0 (Protein Subunits); 0 (Superantigens); 0 (Tumor Necrosis Factor-alpha); 0 (enterotoxin F, Staphylococcal); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go)
[Em] Mês de entrada:0407
[Cu] Atualização por classe:091119
[Lr] Data última revisão:
091119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040629
[St] Status:MEDLINE



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