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[PMID]:29460640
[Au] Autor:Sullivan A; Watkinson J; Waddington J; Park BK; Naisbitt DJ
[Ad] Endereço:a MRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology , The University of Liverpool , Liverpool , England.
[Ti] Título:Implications of HLA-allele associations for the study of type IV drug hypersensitivity reactions.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):261-274, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Type IV drug hypersensitivity remains an important clinical problem and an obstacle to the development of new drugs. Several forms of drug hypersensitivity are associated with expression of specific HLA alleles. Furthermore, drug-specific T-lymphocytes have been isolated from patients with reactions. Despite this, controversy remains as to how drugs interact with immune receptors to stimulate a T-cell response. Areas covered: This article reviews the pathways of T-cell activation by drugs and how the ever increasing number of associations between expression of HLA alleles and susceptibility to hypersensitivity is impacting on our research effort to understanding this form of iatrogenic disease. Expert opinion: For a drug to activate a T-cell, a complex is formed between HLA molecules, an HLA binding peptide, the drug and the T-cell receptor. T-cell responses can involve drugs and stable or reactive metabolites bound covalently or non-covalently to any component of this complex. Recent research has linked the HLA associations to the disease through the characterization of drug-specific T-cell responses restricted to specific alleles. However, there is now a need to identify the additional genetic or environment factors that determine susceptibility and use our increased knowledge to develop predictive immunogenicity tests that offer benefit to Pharma developing new drugs.
[Mh] Termos MeSH primário: Hipersensibilidade a Drogas/imunologia
Antígenos HLA/imunologia
Hipersensibilidade Tardia/induzido quimicamente
[Mh] Termos MeSH secundário: Alelos
Hipersensibilidade a Drogas/genética
Predisposição Genética para Doença
Seres Humanos
Hipersensibilidade Tardia/genética
Hipersensibilidade Tardia/imunologia
Ativação Linfocitária/efeitos dos fármacos
Ativação Linfocitária/imunologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA Antigens)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1441285


  2 / 104462 MEDLINE  
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[PMID]:29381830
[Au] Autor:Sioud M
[Ad] Endereço:Department of Cancer Immunology, Oslo University Hospital, The Norwegian Radium Hospital, Montebello, Oslo, Norway.
[Ti] Título:T-cell cross-reactivity may explain the large variation in how cancer patients respond to checkpoint inhibitors.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The therapeutic use of the immune system to specifically attack tumours has been a long-standing vision among tumour immunologists. Recently, the use of checkpoint inhibitors to turn-off immunosuppressive signals has proven to be effective in enhancing T-cell reactivity against patient-specific neoantigens, resulting from somatic mutations. Several of the identified T-cell epitopes share similarity with common bacterial and viral antigens, suggesting the involvement of pre-existing microbial cross-reactive T cells in rapid and durable tumour regression seen in some patients. This notion of T-cell cross-reactivity is further supported by the findings that intestinal bacteria can influence checkpoint-blockade therapy. Moreover, early data indicate the presence of such T cells in long-term survival breast cancer patients. This review highlights the main challenges for cancer immunotherapy and discusses the potential contribution of T-cell cross-reactivity in cancer immunotherapy and whether it can be used as a biomarker to predict the responsiveness to checkpoint inhibitors.
[Mh] Termos MeSH primário: Reações Cruzadas/imunologia
Imunoterapia/métodos
Neoplasias/imunologia
Neoplasias/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígenos de Bactérias/imunologia
Antígenos de Neoplasias/imunologia
Antígenos Virais/imunologia
Biomarcadores Tumorais/imunologia
Antígeno CTLA-4/antagonistas & inibidores
Células Dendríticas/imunologia
Epitopos de Linfócito T/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptores Imunológicos/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Antigens, Neoplasm); 0 (Antigens, Viral); 0 (Biomarkers, Tumor); 0 (CTLA-4 Antigen); 0 (Epitopes, T-Lymphocyte); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (TIGIT protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12643


  3 / 104462 MEDLINE  
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[PMID]:28453847
[Au] Autor:Khoury G; Fromentin R; Solomon A; Hartogensis W; Killian M; Hoh R; Somsouk M; Hunt PW; Girling V; Sinclair E; Bacchetti P; Anderson JL; Hecht FM; Deeks SG; Cameron PU; Chomont N; Lewin SR
[Ad] Endereço:The Peter Doherty Institute for Infection and Immunity, University of Melbourne and Royal Melbourne Hospital, Australia.
[Ti] Título:Human Immunodeficiency Virus Persistence and T-Cell Activation in Blood, Rectal, and Lymph Node Tissue in Human Immunodeficiency Virus-Infected Individuals Receiving Suppressive Antiretroviral Therapy.
[So] Source:J Infect Dis;215(6):911-919, 2017 03 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Immune activation and inflammation remain elevated in human immunodeficiency virus (HIV)-infected individuals receiving antiretroviral therapy (ART) and may contribute to HIV persistence. Methods: Using flow cytometry expression of CD38, HLA-DR and PD-1 were measured in blood (n = 48), lymph node (LN; n = 9), and rectal tissue (n = 17) from virally suppressed individuals. Total and integrated HIV DNA, 2-LTR circles, and cell-associated unspliced HIV RNA were quantified. Results: CD4+ T cells from rectal tissue had a higher frequency of integrated HIV DNA compared with blood (4.26 fold-change in DNA; 95% confidence interval [CI] = 2.61-7.00; P < .001) and LN (2.32 fold-change in DNA; 95% CI = 1.22-4.41; P = .01). In rectal tissue, there were positive associations between integrated HIV DNA with PD-1+ CD4+ T-cells (1.44 fold-change in integrated HIV DNA per 10-unit increase in PD-1+ CD4+ T cells; 95% CI = 1.01-2.05; P = .045) and CD38+HLA-DR+ CD8+ T cells (1.40 fold-change in integrated HIV DNA per 1-unit increase in CD38+HLA-DR+ CD8+ T cells; 95% CI = 1.05-1.86; P = .02). Both associations were independent of current and nadir CD4+ T-cell counts. Conclusions: During ART, rectal tissue is an important reservoir for HIV persistence with a high frequency of activated CD4+ and CD8+ T cells. PD-1 may represent a marker of HIV persistence in rectal tissue.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Infecções por HIV/tratamento farmacológico
Infecções por HIV/imunologia
Ativação Linfocitária
[Mh] Termos MeSH secundário: Terapia Antirretroviral de Alta Atividade
Austrália
Biomarcadores/metabolismo
Contagem de Linfócito CD4
Estudos Transversais
DNA Viral/sangue
Feminino
HIV-1/imunologia
Antígenos HLA-DR/análise
Seres Humanos
Linfonodos/imunologia
Masculino
Meia-Idade
Receptor de Morte Celular Programada 1/metabolismo
Reto/imunologia
Análise de Regressão
Fatores Sexuais
Estados Unidos
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (DNA, Viral); 0 (HLA-DR Antigens); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jix039


  4 / 104462 MEDLINE  
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[PMID]:28465009
[Au] Autor:Dong G; Kalifa R; Nath PR; Babichev Y; Gelkop S; Isakov N
[Ad] Endereço:The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences and the Cancer Research Center, Ben Gurion University of the Negev, P.O.B. 653, Beer Sheva 84105, Israel. Electronic address: gdong@upenn.edu.
[Ti] Título:Crk adaptor proteins regulate CD3ζ chain phosphorylation and TCR/CD3 down-modulation in activated T cells.
[So] Source:Cell Signal;36:117-126, 2017 Aug.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:T cell receptor (TCR) recognition of a peptide antigen in the context of MHC molecules initiates positive and negative cascades that regulate T cell activation, proliferation and differentiation, and culminate in the acquisition of effector T cell functions. These processes are a prerequisite for the induction of specific T cell-mediated adaptive immune responses. A key event in the activation of TCR-coupled signaling pathways is the phosphorylation of tyrosine residues within the cytoplasmic tails of the CD3 subunits, predominantly CD3ζ. These transiently formed phosphotyrosyl epitopes serve as docking sites for SH2-domain containing effector molecules, predominantly the ZAP70 protein tyrosine kinase, which is critical for signal propagation. We found that CrkI and CrkII adaptor proteins also interact with CD3ζ in TCR activated-, but not in resting-, T cells. Crk binding to CD3ζ was independent of ZAP70 and also occurred in ZAP70-deficient T cells. Binding was mediated by Crk-SH2 domain interaction with phosphotyrosine-containing motifs on CD3ζ, via a direct physical interaction, as demonstrated by Far-Western blot. CrkII binding to CD3ζ could also be demonstrated in a heterologous system, where coexpression of a catalytically active Lck was used to phosphorylate the CD3ζ chain. TCR activation-induced Crk binding to CD3ζ resulted in increased and prolonged phosphorylation of CD3ζ, as well as ZAP70 and LAT, suggesting a positive role for CrkI/II binding to CD3ζ in regulation of TCR-coupled signaling pathways. Furthermore, Crk-dependent increased phosphorylation of CD3ζ coincided with inhibition of TCR downmodulation, supporting a positive role for Crk adaptor proteins in TCR-mediated signal amplification.
[Mh] Termos MeSH primário: Complexo CD3/metabolismo
Regulação para Baixo
Ativação Linfocitária
Proteínas Proto-Oncogênicas c-crk/metabolismo
Receptores de Antígenos de Linfócitos T/metabolismo
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos/metabolismo
Células COS
Cercopithecus aethiops
Reagentes para Ligações Cruzadas/farmacologia
Regulação para Baixo/efeitos dos fármacos
Seres Humanos
Células Jurkat
Ativação Linfocitária/efeitos dos fármacos
Camundongos
Peso Molecular
Fosforilação/efeitos dos fármacos
Fosfotirosina/metabolismo
Ligação Proteica/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-crk/química
Linfócitos T/efeitos dos fármacos
Vanadatos/farmacologia
Proteína-Tirosina Quinase ZAP-70/metabolismo
Domínios de Homologia de src
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD3 Complex); 0 (CRK protein, human); 0 (Cross-Linking Reagents); 0 (Proto-Oncogene Proteins c-crk); 0 (Receptors, Antigen, T-Cell); 0 (pervanadate); 21820-51-9 (Phosphotyrosine); 3WHH0066W5 (Vanadates); EC 2.7.10.2 (ZAP-70 Protein-Tyrosine Kinase); EC 2.7.10.2 (ZAP70 protein, human)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:27773685
[Au] Autor:Fehniger TA; Cooper MA
[Ad] Endereço:Department of Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: tfehnige@wustl.edu.
[Ti] Título:Harnessing NK Cell Memory for Cancer Immunotherapy.
[So] Source:Trends Immunol;37(12):877-888, 2016 12.
[Is] ISSN:1471-4981
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Due to their ability to kill cancer cells and produce proinflammatory cytokines, natural killer (NK) cells have long been of clinical interest for their antitumor properties. The recent discovery of NK cell memory demonstrates that NK cell functions, and potentially antitumor responses, can be enhanced long term. Following nonspecific activation with the cytokines IL-12, IL-15, and IL-18 or in response to antigens or cytomegalovirus (CMV), human and mouse NK cells exhibit stable, enhanced functional responses with phenotypic and molecular changes. Here we review mechanisms driving the differentiation of NK cell memory-like properties, evidence for antitumor activity, and the challenges and opportunities in harnessing memory-like NK cells for cancer immunotherapy.
[Mh] Termos MeSH primário: Vacinas Anticâncer/imunologia
Memória Imunológica
Imunoterapia Adotiva/métodos
Células Matadoras Naturais/imunologia
Subpopulações de Linfócitos/imunologia
Neoplasias/terapia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Citocinas/metabolismo
Citomegalovirus/imunologia
Citotoxicidade Imunológica
Seres Humanos
Mediadores da Inflamação/metabolismo
Células Matadoras Naturais/transplante
Ativação Linfocitária
Subpopulações de Linfócitos/transplante
Camundongos
Neoplasias/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cancer Vaccines); 0 (Cytokines); 0 (Inflammation Mediators)
[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:161025
[St] Status:MEDLINE


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[PMID]:27775159
[Au] Autor:Arévalo MT; Li J; Diaz-Arévalo D; Chen Y; Navarro A; Wu L; Yan Y; Zeng M
[Ad] Endereço:Center of Emphasis in Infectious Diseases, Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, TX, USA.
[Ti] Título:A dual purpose universal influenza vaccine candidate confers protective immunity against anthrax.
[So] Source:Immunology;150(3):276-289, 2017 03.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Preventive influenza vaccines must be reformulated annually because of antigen shift and drift of circulating influenza viral strains. However, seasonal vaccines do not always match the circulating strains, and there is the ever-present threat that avian influenza viruses may adapt to humans. Hence, a universal influenza vaccine is needed to provide protective immunity against a broad range of influenza viruses. We designed an influenza antigen consisting of three tandem M2e repeats plus HA2, in combination with a detoxified anthrax oedema toxin delivery system (EFn plus PA) to enhance immune responses. The EFn-3×M2e-HA2 plus PA vaccine formulation elicited robust, antigen-specific, IgG responses; and was protective against heterologous influenza viral challenge when intranasally delivered to mice three times. Moreover, use of the detoxified anthrax toxin system as an adjuvant had the additional benefit of generating protective immunity against anthrax. Hence, this novel vaccine strategy could potentially address two major emerging public health and biodefence threats.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/administração & dosagem
Antraz/imunologia
Antígenos de Bactérias/administração & dosagem
Toxinas Bacterianas/administração & dosagem
Vacinas contra Influenza/imunologia
Influenza Humana/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antibacterianos/sangue
Anticorpos Antivirais/sangue
Bioterrorismo
Células Cultivadas
Citocinas/metabolismo
Seres Humanos
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Orthomyxoviridae/imunologia
Linfócitos T/microbiologia
Linfócitos T/virologia
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Antibodies, Bacterial); 0 (Antibodies, Viral); 0 (Antigens, Bacterial); 0 (Bacterial Toxins); 0 (Cytokines); 0 (Influenza Vaccines); 0 (anthrax toxin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12683


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[PMID]:29360859
[Au] Autor:Zhou J; Bethune MT; Malkova N; Sutherland AM; Comin-Anduix B; Su Y; Baltimore D; Ribas A; Heath JR
[Ad] Endereço:NanoSystems Biology Cancer Center, California Institute of Technology, Pasadena, California, United States of America.
[Ti] Título:A kinetic investigation of interacting, stimulated T cells identifies conditions for rapid functional enhancement, minimal phenotype differentiation, and improved adoptive cell transfer tumor eradication.
[So] Source:PLoS One;13(1):e0191634, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:For adoptive cell transfer (ACT) immunotherapy of tumor-reactive T cells, an effective therapeutic outcome depends upon cell dose, cell expansion in vivo through a minimally differentiated phenotype, long term persistence, and strong cytolytic effector function. An incomplete understanding of the biological coupling between T cell expansion, differentiation, and response to stimulation hinders the co-optimization of these factors. We report on a biophysical investigation of how the short-term kinetics of T cell functional activation, through molecular stimulation and cell-cell interactions, competes with phenotype differentiation. T cells receive molecular stimulation for a few minutes to a few hours in bulk culture. Following this priming period, the cells are then analyzed at the transcriptional level, or isolated as single cells, with continuing molecular stimulation, within microchambers for analysis via 11-plex secreted protein assays. We resolve a rapid feedback mechanism, promoted by T cell-T cell contact interactions, which strongly amplifies T cell functional performance while yielding only minimal phenotype differentiation. When tested in mouse models of ACT, optimally primed T cells lead to complete tumor eradication. A similar kinetic process is identified in CD8+ and CD4+ T cells collected from a patient with metastatic melanoma.
[Mh] Termos MeSH primário: Transferência Adotiva
Imunofenotipagem
Neoplasias/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Citometria de Fluxo
Xenoenxertos
Seres Humanos
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191634


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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 / 104462 MEDLINE  
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[PMID]:28747344
[Au] Autor:Burbage M; Keppler SJ; Montaner B; Mattila PK; Batista FD
[Ad] Endereço:Lymphocyte Interaction Laboratory, Francis Crick Institute, London NW1 1AT, United Kingdom.
[Ti] Título:The Small Rho GTPase TC10 Modulates B Cell Immune Responses.
[So] Source:J Immunol;199(5):1682-1695, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rho family GTPases regulate diverse cellular events, such as cell motility, polarity, and vesicle traffic. Although a wealth of data exists on the canonical Rho GTPases RhoA, Rac1, and Cdc42, several other family members remain poorly studied. In B cells, we recently demonstrated a critical role for Cdc42 in plasma cell differentiation. In this study, we focus on a close homolog of Cdc42, TC10 (also known as RhoQ), and investigate its physiological role in B cells. By generating a TC10-deficient mouse model, we show that despite reduced total B cell numbers, B cell development in these mice occurs normally through distinct developmental stages. Upon immunization, IgM levels were reduced and, upon viral infection, germinal center responses were defective in TC10-deficient mice. BCR signaling was mildly affected, whereas cell migration remained normal in TC10-deficient B cells. Furthermore, by generating a TC10/Cdc42 double knockout mouse model, we found that TC10 can compensate for the lack of Cdc42 in TLR-induced cell activation and proliferation, so the two proteins play partly redundant roles. Taken together, by combining in vivo and in vitro analysis using TC10-deficient mice, we define the poorly studied Rho GTPase TC10 as an immunomodulatory molecule playing a role in physiological B cell responses.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Infecções por Orthomyxoviridae/imunologia
Vaccinia/imunologia
Proteína cdc42 de Ligação ao GTP/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular
Células Cultivadas
Centro Germinativo/imunologia
Imunomodulação
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Antígenos de Linfócitos B/metabolismo
Transdução de Sinais
Proteína cdc42 de Ligação ao GTP/genética
Proteínas rho de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdc42 protein, mouse); 0 (Receptors, Antigen, B-Cell); EC 3.6.1.- (Rhoq protein, mouse); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602167


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[PMID]:29304125
[Au] Autor:Barisone GA; O'Donnell RT; Ma Y; Abuhay MW; Lundeberg K; Gowda S; Tuscano JM
[Ad] Endereço:Division of Hematology and Oncology, Department of Internal Medicine, University of California Davis, Sacramento, California, United States of America.
[Ti] Título:A purified, fermented, extract of Triticum aestivum has lymphomacidal activity mediated via natural killer cell activation.
[So] Source:PLoS One;13(1):e0190860, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Non-Hodgkin lymphoma (NHL) affects over 400,000 people in the United States; its incidence increases with age. Treatment options are numerous and expanding, yet efficacy is often limited by toxicity, particularly in the elderly. Nearly 70% patients eventually die of the disease. Many patients explore less toxic alternative therapeutics proposed to boost anti-tumor immunity, despite a paucity of rigorous scientific data. Here we evaluate the lymphomacidal and immunomodulatory activities of a protein fraction isolated from fermented wheat germ. Fermented wheat germ extract was produced by fermenting wheat germ with Saccharomyces cerevisiae. A protein fraction was tested for lymphomacidal activity in vitro using NHL cell lines and in vivo using mouse xenografts. Mechanisms of action were explored in vitro by evaluating apoptosis and cell cycle and in vivo by immunophenotyping and measurement of NK cell activity. Potent lymphomacidal activity was observed in a panel of NHL cell lines and mice bearing NHL xenografts. This activity was not dependent on wheat germ agglutinin or benzoquinones. Fermented wheat germ proteins induced apoptosis in NHL cells, and augmented immune effector mechanisms, as measured by NK cell killing activity, degranulation and production of IFNγ. Fermented wheat germ extract can be easily produced and is efficacious in a human lymphoma xenograft model. The protein fraction is quantifiable and more potent, shows direct pro-apoptotic properties, and enhances immune-mediated tumor eradication. The results presented herein support the novel concept that proteins in fermented wheat germ have direct pro-apoptotic activity on lymphoma cells and augment host immune effector mechanisms.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Células Matadoras Naturais/imunologia
Ativação Linfocitária/efeitos dos fármacos
Linfoma não Hodgkin/patologia
Extratos Vegetais/farmacologia
Triticum/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Feminino
Fermentação
Seres Humanos
Linfoma não Hodgkin/imunologia
Camundongos
Camundongos Nus
Proteínas de Plantas/farmacologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Plant Extracts); 0 (Plant Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190860



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