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[PMID]:29232953
[Au] Autor:Wang L; Zhang Y; Wang D; Wang M; Wang Y; Feng J
[Ad] Endereço:Research and Development Center of Biorational Pesticide, Northwest A&F University , Yangling 712100, Shaanxi, China.
[Ti] Título:Mitochondrial Signs and Subcellular Imaging Provide Insight into the Antifungal Mechanism of Carabrone against Gaeumannomyces graminis var. tritici.
[So] Source:J Agric Food Chem;66(1):81-90, 2018 Jan 10.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Carabrone, a botanical bicyclic sesquiterpenic lactone, has broad-spectrum antifungal activity and is particularly efficient against the devastating phytopathogen Gaeumannomyces graminis var. tritici (Ggt). The antifungal mechanism of carabrone against Ggt, however, remains unclear. The main objective of this study was to investigate the subcellular localization of carabrone in Ggt to gain a better understanding of its mechanism of action. When Ggt was exposed to carabrone (EC value of 28.45 µg/mL) for 7 days, a decline in mitochondrial concentration together with some obvious alternations in mitochondrial structure, including hazy outlines, medullary transitions, excess accumulation of unclear settlings, and vacuolar degeneration, were observed, indicating that carbrone may act on the mitochondria directly. A fluorescent conjugate (TTY) was thus designed and synthesized as a surrogate of carabrone that possessed comparable antifungal activity against Ggt (EC of 33.68 µg/mL). Additionally, a polyclonal antibody specific to carabrone and with a high titer (256 000) was also prepared by immunizing mice. Subsequently, two imaging techniques, the use of the fluorescent conjugate (FC) and immunofluorescence (IF), were applied to determine the subcellular localization of carabrone. Both FC and IF fluorescent signals demonstrated its mitochondrial localization with a Pearson's coefficient of 0.83 for FC and 0.86 for IF. These results imply that carabrone exerts its antifungal activity against Ggt by interfering with mitochondrial function.
[Mh] Termos MeSH primário: Antifúngicos/farmacologia
Ascomicetos/efeitos dos fármacos
Fungicidas Industriais/farmacologia
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antifúngicos/química
Ascomicetos/metabolismo
Feminino
Imunofluorescência/métodos
Fungicidas Industriais/síntese química
Fungicidas Industriais/química
Haptenos/química
Hifas/efeitos dos fármacos
Hifas/ultraestrutura
Cinética
Camundongos Endogâmicos BALB C
Mitocôndrias/ultraestrutura
Imagem Molecular/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antifungal Agents); 0 (Fungicides, Industrial); 0 (Haptens)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b03913


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[PMID]:28747341
[Au] Autor:Suwanpradid J; Shih M; Pontius L; Yang B; Birukova A; Guttman-Yassky E; Corcoran DL; Que LG; Tighe RM; MacLeod AS
[Ad] Endereço:Department of Dermatology, Duke University, Durham, NC 27710.
[Ti] Título:Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.
[So] Source:J Immunol;199(5):1827-1834, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The innate immune components that modulate allergic contact hypersensitivity (CHS) responses are poorly defined. Using human skin from contact dermatitis patients and a mouse model of CHS, we find that hapten allergens disrupt the Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mono/MΦ), which renders those cells ineffectual in suppressing skin inflammation. Mice lacking Arg1 in MΦ develop increased CHS characterized by elevated ear thickening, mono/MΦ-dominated dermal inflammation, and increased iNOS and IL-6 expression compared with control mice. Treatment of Arg1 ; LysMCre mice with a selective NOS inhibitor or knockout of , encoding iNOS, significantly ameliorates CHS. Our findings suggest a critical role for Arg1 in mono/MΦ in suppressing CHS through dampening expression. These results support that increasing Arg1 may be a potential therapeutic avenue in treating allergic contact dermatitis.
[Mh] Termos MeSH primário: Arginase/metabolismo
Dermatite Alérgica de Contato/imunologia
Macrófagos/imunologia
Óxido Nítrico Sintase Tipo II/metabolismo
Pele/imunologia
[Mh] Termos MeSH secundário: Alérgenos/imunologia
Animais
Arginase/genética
Células Cultivadas
Dermatite Alérgica de Contato/genética
Modelos Animais de Doenças
Feminino
Haptenos/imunologia
Seres Humanos
Imunidade Inata
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Óxido Nítrico Sintase Tipo II/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Allergens); 0 (Haptens); 0 (Interleukin-6); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase I, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700739


  3 / 7328 MEDLINE  
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[PMID]:28972093
[Au] Autor:Cho Y; Kwon D; Kang SJ
[Ad] Endereço:Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 34141, Republic of Korea.
[Ti] Título:The Cooperative Role of CD326 and CD11b Dendritic Cell Subsets for a Hapten-Induced Th2 Differentiation.
[So] Source:J Immunol;199(9):3137-3146, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dendritic cells (DCs) play a critical role in directing immune responses. Previous studies have identified a variety of DC subsets and elucidated their context-dependent functions that parallel those of effector Th cell subsets. However, little is known about the DC subsets responsible for differentiation of Th2 cells governing allergic contact dermatitis. In this study, we sought to determine the DC subset(s) that mediate Th2 priming in hapten-sensitized mice. We induced hapten-specific Th2 differentiation by sensitizing the mice with a single application of FITC dissolved in acetone:dibutyl phthalate, and traced the immune cells responsible for inducing the Th2 differentiation process at the primary stimulation, enabling us to track Th2 priming in vivo and to delete basophils and specific DC subsets. Our analysis revealed that IL-4 was produced in vivo as early as day 3 from CD4 T cells with a single application of FITC. Basophils, despite producing IL-4 1 d earlier than T cells, were found to be dispensable for Th2 differentiation. Instead, we demonstrated that CD326 dermal DCs and Langerhans cells were redundantly required for FITC-induced Th2 differentiation in vivo. Moreover, the cooperation of CD326 Langerhans cells and CD11b DCs differentiated naive T cells into Th2 cells in vitro. Collectively, our findings highlight at least two DC subsets that play a critical role in polarizing naive CD4 T cells to Th2 cells and support a two-hit model for Th2 differentiation.
[Mh] Termos MeSH primário: Antígeno CD11b/imunologia
Diferenciação Celular/efeitos dos fármacos
Molécula de Adesão da Célula Epitelial/imunologia
Haptenos/farmacologia
Células de Langerhans/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b/genética
Diferenciação Celular/genética
Diferenciação Celular/imunologia
Molécula de Adesão da Célula Epitelial/genética
Interleucina-4/genética
Interleucina-4/imunologia
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Epithelial Cell Adhesion Molecule); 0 (Haptens); 207137-56-2 (Interleukin-4)
[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:171004
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601262


  4 / 7328 MEDLINE  
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[PMID]:28794018
[Au] Autor:Paust S; Blish CA; Reeves RK
[Ad] Endereço:Department of Pediatrics, Center for Human Immunobiology, Texas Children's Hospital, and Department of Pathology and Immunology and Department of Molecular Virology and Microbiology, Digestive Disease Center, Baylor College of Medicine, Houston, Texas, USA silke.paust@bcm.edu rreeves@bidmc.harvard.e
[Ti] Título:Redefining Memory: Building the Case for Adaptive NK Cells.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Classically, natural killer (NK) cells have been defined by nonspecific innate killing of virus-infected and tumor cells. However, burgeoning evidence suggests that the functional repertoire of NK cells is far more diverse than has been previously appreciated, thus raising the possibility that there may be unexpected functional specialization and even adaptive capabilities among NK cell subpopulations. Some of the first evidence that NK cells respond in an antigen-specific fashion came from experiments revealing that subpopulations of murine NK cells were able to respond to a specific murine cytomegalovirus (MCMV) protein and that in the absence of T and B cells, murine NK cells also mediated adaptive immune responses to a secondary challenge with specific haptens. These data have been followed by demonstrations of NK cell memory of viruses and viral antigens in mice and primates. Herein, we discuss different forms of NK cell antigen specificity and how these responses may be tuned to specific viral pathogens, and we provide assessment of the current literature that may explain molecular mechanisms of the novel phenomenon of NK cell memory.
[Mh] Termos MeSH primário: Imunidade Inata
Memória Imunológica
Células Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Antígenos Virais/imunologia
Epitopos
Haptenos
Seres Humanos
Camundongos
Muromegalovirus/química
Muromegalovirus/imunologia
Primatas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Viral); 0 (Epitopes); 0 (Haptens)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE


  5 / 7328 MEDLINE  
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[PMID]:28753003
[Au] Autor:Thyparambil AA; Abramyan TM; Bazin I; Guiseppi-Elie A
[Ad] Endereço:Center for Bioelectronics, Biosensors and Biochips (C3B), Texas A&M University , College Station, Texas 77843, United States.
[Ti] Título:Site of Tagging Influences the Ochratoxin Recognition by Peptide NFO4: A Molecular Dynamics Study.
[So] Source:J Chem Inf Model;57(8):2035-2044, 2017 Aug 28.
[Is] ISSN:1549-960X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Molecular recognition by synthetic peptides is growing in importance in the design of biosensing elements used in the detection and monitoring of a wide variety of hapten bioanlaytes. Conferring specificity via bioimmobilization and subsequent recovery and purification of such sensing elements are aided by the use of affinity tags. However, the tag and its site of placement can potentially compromise the hapten recognition capabilities of the peptide, necessitating a detailed experimental characterization and optimization of the tagged molecular recognition entity. The objective of this study was to assess the impact of site-specific tags on a native peptide's fold and hapten recognition capabilities using an advanced molecular dynamics (MD) simulation approach involving bias-exchange metadynamics and Markov State Models. The in-solution binding preferences of affinity tagged NFO4 (VYMNRKYYKCCK) to chlorinated (OTA) and non-chlorinated (OTB) analogues of ochratoxin were evaluated by appending hexa-histidine tags (6× His-tag) to the peptide's N-terminus (NterNFO4) or C-terminus (CterNFO4), respectively. The untagged NFO4 (NFO4), previously shown to bind with high affinity and selectivity to OTA, served as the control. Results indicate that the addition of site-specific 6× His-tags altered the peptide's native fold and the ochratoxin binding mechanism, with the influence of site-specific affinity tags being most evident on the peptide's interaction with OTA. The tags at the N-terminus of NFO4 preserved the native fold and actively contributed to the nonbonded interactions with OTA. In contrast, the tags at the C-terminus of NFO4 altered the native fold and were agnostic in its nonbonded interactions with OTA. The tags also increased the penalty associated with solvating the peptide-OTA complex. Interestingly, the tags did not significantly influence the nonbonded interactions or the penalty associated with solvating the peptide-OTB complex. Overall, the combined contributions of nonbonded interaction and solvation penalty were responsible for the retention of the native hapten recognition capabilities in NterNFO4 and compromised native recognition capabilities in CterNFO4. Advanced MD approaches can thus provide structural and energetic insights critical to evaluate the impact of site-specific tags and may aid in the selection and optimization of the binding preferences of a specific biosensing element.
[Mh] Termos MeSH primário: Simulação de Dinâmica Molecular
Ocratoxinas/metabolismo
Oligopeptídeos/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sítios de Ligação
Haptenos/metabolismo
Histidina/química
Ocratoxinas/química
Oligopeptídeos/química
Ligação Proteica
Conformação Proteica
Dobramento de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Haptens); 0 (Ochratoxins); 0 (Oligopeptides); 4QD397987E (Histidine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jcim.7b00312


  6 / 7328 MEDLINE  
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[PMID]:28709828
[Au] Autor:Wenthur CJ; Cai X; Ellis BA; Janda KD
[Ad] Endereço:Departments of Chemistry and Immunology, The Scripps Research Institute, La Jolla, CA 92037, United States.
[Ti] Título:Augmenting the efficacy of anti-cocaine catalytic antibodies through chimeric hapten design and combinatorial vaccination.
[So] Source:Bioorg Med Chem Lett;27(16):3666-3668, 2017 08 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Given the need for further improvements in anti-cocaine vaccination strategies, a chimeric hapten (GNET) was developed that combines chemically-stable structural features from steady-state haptens with the hydrolytic functionality present in transition-state mimetic haptens. Additionally, as a further investigation into the generation of an improved bifunctional antibody pool, sequential vaccination with steady-state and transition-state mimetic haptens was undertaken. While GNET induced the formation of catalytically-active antibodies, it did not improve overall behavioral efficacy. In contrast, the resulting pool of antibodies from GNE/GNT co-administration demonstrated intermediate efficacy as compared to antibodies developed from either hapten alone. Overall, improved antibody catalytic efficiency appears necessary to achieve the synergistic benefits of combining cocaine hydrolysis with peripheral sequestration.
[Mh] Termos MeSH primário: Anticorpos Catalíticos/imunologia
Cocaína/imunologia
Haptenos/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Catalíticos/sangue
Anticorpos Catalíticos/metabolismo
Catálise
Cocaína/química
Cocaína/farmacologia
Ensaio de Imunoadsorção Enzimática
Haptenos/química
Imunoglobulina G/sangue
Locomoção/efeitos dos fármacos
Radioimunoensaio
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Catalytic); 0 (Haptens); 0 (Immunoglobulin G); I5Y540LHVR (Cocaine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE


  7 / 7328 MEDLINE  
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[PMID]:28695285
[Au] Autor:Illing PT; Purcell AW; McCluskey J
[Ad] Endereço:Infection and Immunity Program & Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, 3800, Australia.
[Ti] Título:The role of HLA genes in pharmacogenomics: unravelling HLA associated adverse drug reactions.
[So] Source:Immunogenetics;69(8-9):617-630, 2017 Aug.
[Is] ISSN:1432-1211
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic polymorphism in the genes encoding the human leukocyte antigen (HLA) molecules enables presentation of a wide range peptide ligands thus maximising immune surveillance of pathogens. A consequence of the diversification of the HLA Ag-binding pocket is the enhanced opportunity for off-target binding of small drugs by HLA molecules, with subsequent immune reactivity. These potential off-target interactions are 'set up' to generate T cell-mediated adverse drug reactions even though the precise mechanisms of most HLA-drug interactions are still poorly understood. The association between abacavir hypersensitivity syndrome and HLA-B*57:01 is one exception that has been resolved at a molecular and mechanistic level. Here, we explore the road to understanding the interaction between abacavir and the HLA-B*57:01 molecule and review the current state of understanding of interactions between other drugs and HLA molecules implicated in adverse drug reactions, which appear to involve multiple mechanisms. The continued expansion of the pharmacopoeia generates an imperative to understand these interactions at the molecular level in order to prevent the continued burden on individuals and the health care system.
[Mh] Termos MeSH primário: Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/genética
Antígenos HLA/genética
Farmacogenética
[Mh] Termos MeSH secundário: Alopurinol/efeitos adversos
Carbamazepina/efeitos adversos
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/imunologia
Haptenos/imunologia
Seres Humanos
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA Antigens); 0 (Haptens); 33CM23913M (Carbamazepine); 63CZ7GJN5I (Allopurinol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1007/s00251-017-1007-5


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[PMID]:28687658
[Au] Autor:Gibson A; Faulkner L; Lichtenfels M; Ogese M; Al-Attar Z; Alfirevic A; Esser PR; Martin SF; Pirmohamed M; Park BK; Naisbitt DJ
[Ad] Endereço:Department of Molecular and Clinical Pharmacology, Medical Research Council Centre for Drug Safety Science, University of Liverpool, Liverpool L69 3GE, United Kingdom.
[Ti] Título:The Effect of Inhibitory Signals on the Priming of Drug Hapten-Specific T Cells That Express Distinct Vß Receptors.
[So] Source:J Immunol;199(4):1223-1237, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Drug hypersensitivity involves the activation of T cells in an HLA allele-restricted manner. Because the majority of individuals who carry HLA risk alleles do not develop hypersensitivity, other parameters must control development of the drug-specific T cell response. Thus, we have used a T cell-priming assay and nitroso sulfamethoxazole (SMX-NO) as a model Ag to investigate the activation of specific TCR Vß subtypes, the impact of programmed death -1 (PD-1), CTL-associated protein 4 (CTLA4), and T cell Ig and mucin domain protein-3 (TIM-3) coinhibitory signaling on activation of naive and memory T cells, and the ability of regulatory T cells (Tregs) to prevent responses. An expansion of the TCR repertoire was observed for nine Vß subtypes, whereas spectratyping revealed that SMX-NO-specific T cell responses are controlled by public TCRs present in all individuals alongside private TCR repertoires specific to each individual. We proceeded to evaluate the extent to which the activation of these TCR Vß-restricted Ag-specific T cell responses is governed by regulatory signals. Blockade of PD-L1/CTLA4 signaling dampened activation of SMX-NO-specific naive and memory T cells, whereas blockade of TIM-3 produced no effect. Programmed death-1, CTLA4, and TIM-3 displayed discrete expression profiles during drug-induced T cell activation, and expression of each receptor was enhanced on dividing T cells. Because these receptors are also expressed on Tregs, Treg-mediated suppression of SMX-NO-induced T cell activation was investigated. Tregs significantly dampened the priming of T cells. In conclusion, our findings demonstrate that distinct TCR Vß subtypes, dysregulation of coinhibitory signaling pathways, and dysfunctional Tregs may influence predisposition to hypersensitivity.
[Mh] Termos MeSH primário: Haptenos/imunologia
Ativação Linfocitária
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Linfócitos T CD4-Positivos/imunologia
Antígeno CTLA-4/metabolismo
Hipersensibilidade a Drogas
Receptor Celular 2 do Vírus da Hepatite A/metabolismo
Seres Humanos
Memória Imunológica
Receptor de Morte Celular Programada 1/metabolismo
Receptores de Antígenos de Linfócitos T alfa-beta/antagonistas & inibidores
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/metabolismo
Sulfametoxazol/análogos & derivados
Sulfametoxazol/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (HAVCR2 protein, human); 0 (Haptens); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Antigen, T-Cell, alpha-beta); 131549-85-4 (4-nitrososulfamethoxazole); JE42381TNV (Sulfamethoxazole)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170709
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602029


  9 / 7328 MEDLINE  
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[PMID]:28598600
[Au] Autor:Ceballos-Alcantarilla E; Abad-Somovilla A; Agulló C; Abad-Fuentes A; Mercader JV
[Ad] Endereço:Department of Organic Chemistry, Universitat de València , Doctor Moliner 50, 46100 Burjassot, València, Spain.
[Ti] Título:Protein-Free Hapten-Carbon Nanotube Constructs Induce the Secondary Immune Response.
[So] Source:Bioconjug Chem;28(6):1630-1638, 2017 Jun 21.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Carbon nanotubes are novel technological tools with multiple applications. The interaction between such nanoparticles and living organisms is nowadays a matter of keen research by academic and private institutions. In this study, carbon nanotube constructs were investigated as delivery vehicles for immunostimulation and induction of the secondary immune response to a small organic molecule, namely, a hapten. Two types of nanoconstructs were prepared: on one hand, carbon nanotubes carrying a protein bioconjugate of a hapten covalently linked to the carbon surface, and on the other hand, covalent carbon nanotube constructs of the same model chemical compound without the carrier protein. Nanotube vehicles carrying a hapten-protein bioconjugate were demonstrated to stimulate the immune system and to induce a strong primary immune response against the hapten with as low as 0.1 µg of the model chemical. The influence of the different elements of those nanoconstructs over the immune response was investigated to better understand the molecular mechanisms that are involved. As expected, the presence of the carrier protein was shown to be necessary in order to trigger the immune response. Interestingly, we found that a remarkable secondary immune response to the model organic compound occurred in the absence of a carrier protein. Additionally, a satisfactory adjuvant effect of carbon nanotubes was observed and a potent immune response was elicited without employing an oil-based adjuvant.
[Mh] Termos MeSH primário: Haptenos/imunologia
Imunização
Nanotubos de Carbono/química
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos
Proteínas de Transporte
Haptenos/química
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Carrier Proteins); 0 (Haptens); 0 (Nanotubes, Carbon)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1021/acs.bioconjchem.6b00653


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[PMID]:28438900
[Au] Autor:Meng X; Al-Attar Z; Yaseen FS; Jenkins R; Earnshaw C; Whitaker P; Peckham D; French NS; Naisbitt DJ; Park BK
[Ad] Endereço:Medical Research Council Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology, The University of Liverpool, Liverpool L69 3GE, United Kingdom; and.
[Ti] Título:Definition of the Nature and Hapten Threshold of the ß-Lactam Antigen Required for T Cell Activation In Vitro and in Patients.
[So] Source:J Immunol;198(11):4217-4227, 2017 Jun 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Covalent modification of protein by drugs may disrupt self-tolerance, leading to lymphocyte activation. Until now, determination of the threshold required for this process has not been possible. Therefore, we performed quantitative mass spectrometric analyses to define the epitopes formed in tolerant and hypersensitive patients taking the ß-lactam antibiotic piperacillin and the threshold required for T cell activation. A hydrolyzed piperacillin hapten was detected on four lysine residues of human serum albumin (HSA) isolated from tolerant patients. The level of modified Lys ranged from 2.6 to 4.8%. Analysis of plasma from hypersensitive patients revealed the same pattern and levels of modification 1-10 d after the commencement of therapy. Piperacillin-responsive skin-homing CD4 clones expressing an array of Vß receptors were activated in a dose-, time-, and processing-dependent manner; analysis of incubation medium revealed that 2.6% of Lys in HSA was modified when T cells were activated. Piperacillin-HSA conjugates that had levels and epitopes identical to those detected in patients were shown to selectively stimulate additional CD4 clones, which expressed a more restricted Vß repertoire. To conclude, the levels of piperacillin-HSA modification that activated T cells are equivalent to the ones formed in hypersensitive and tolerant patients, which indicates that threshold levels of drug Ag are formed in all patients. Thus, the propensity to develop hypersensitivity is dependent on other factors, such as the presence of T cells within an individual's repertoire that can be activated with the ß-lactam hapten and/or an imbalance in immune regulation.
[Mh] Termos MeSH primário: Antibacterianos/imunologia
Linfócitos T CD4-Positivos/imunologia
Hipersensibilidade a Drogas/imunologia
Epitopos/imunologia
Haptenos/imunologia
Ativação Linfocitária
beta-Lactamas/imunologia
[Mh] Termos MeSH secundário: Adulto
Antibacterianos/administração & dosagem
Antibacterianos/farmacologia
Antígenos/imunologia
Linfócitos T CD4-Positivos/fisiologia
Epitopos/química
Feminino
Haptenos/administração & dosagem
Haptenos/química
Haptenos/metabolismo
Seres Humanos
Tolerância Imunológica
Masculino
Espectrometria de Massas
Piperacilina/administração & dosagem
Piperacilina/imunologia
Piperacilina/metabolismo
Albumina Sérica/química
Albumina Sérica/imunologia
Adulto Jovem
beta-Lactamas/administração & dosagem
beta-Lactamas/metabolismo
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antigens); 0 (Epitopes); 0 (Haptens); 0 (Serum Albumin); 0 (beta-Lactams); X00B0D5O0E (Piperacillin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700209



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