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Pesquisa : D23.050.301.264.894.090 [Categoria DeCS]
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  1 / 1967 MEDLINE  
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[PMID]:28781259
[Au] Autor:Todosenko NM; Khaziakhmatova OG; Yurova KA; Malinina IP; Litvinova LS
[Ad] Endereço:Immanuel Kant Baltic Federal University.
[Ti] Título:[The influence of methylprednisolone on the ability of CD4+CD95+HLA-DR+ T-cells to produce proinflammatory medators in cultures of TCR-activated CD3+CD45RO+ T-lymphocytes from patients with rheumatoid arthritis].
[Ti] Título:Vliianie metilprednizolona na sposobnost' CD4+CD95+HLA-DR+ T-kletok v kul'turakh TCR-aktivirovannykh CD3+CD45RO+ T-limfotsitov bol'nykh revmatoidnym artritom produtsirovat' provospalitel'nye mediatory..
[So] Source:Biomed Khim;63(3):255-265, 2017 May.
[Is] ISSN:2310-6972
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The effect of different concentrations of the glucocorticoid (GC) methylprednisolone (MP) on CD4+CD95+HLA-DR+ T-cells and their ability to produce proinflammatory mediators in cultures of TCR-stimulated CD3+CD45RO+ T-lymphocytes in the in vitro system was investigated. T cells were obtained from healthy donors and patients with rheumatoid arthritis (RA).Under conditions of TCR-activation, MP increased the number of CD4+HLA-DR+CD95+ cells in CD3+CD45RO+ cultures obtained from RA patients and did not change their content in the control group. In general, MP decreased production of proinflammatory factors (IFN-, IL-2, IL-17, IL-21 and TNF-) by TCR-activated CD3+CD45RO+ cells from healthy donors and RA, consistent with the overall immunosuppressive mechanism of GC action. The correlation between CD4+CD45RO+HLA-DR+CD95+ T-cell contents and parameters reflecting production of proinflammatory mediators (IL-17, IL-21 and TNF-) in RA patients indicates maintenance of the pro-inflammatory potential of this T-cell population exposed to GC action. We suggest that relative resistance of CD4+CD45RO+CD95+HLA-DR+ T-cells of RA patients to the suppressor effect of GC leads to maintenance and even enhancement in the functional capacities of autoreactive cells in the pathogenesis of RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Glucocorticoides/farmacologia
Metilprednisolona/farmacologia
[Mh] Termos MeSH secundário: Adulto
Anticorpos/farmacologia
Artrite Reumatoide/patologia
Antígenos CD2/genética
Antígenos CD2/imunologia
Complexo CD3/genética
Complexo CD3/imunologia
Antígenos CD4/genética
Antígenos CD4/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/patologia
Estudos de Casos e Controles
Feminino
Regulação da Expressão Gênica/imunologia
Antígenos HLA-DR/genética
Antígenos HLA-DR/imunologia
Seres Humanos
Interleucina-17/biossíntese
Interleucina-17/imunologia
Interleucina-2/biossíntese
Interleucina-2/imunologia
Interleucinas/biossíntese
Interleucinas/imunologia
Antígenos Comuns de Leucócito/genética
Antígenos Comuns de Leucócito/imunologia
Ativação Linfocitária
Masculino
Cultura Primária de Células
Transdução de Sinais
Fator de Necrose Tumoral alfa/biossíntese
Fator de Necrose Tumoral alfa/imunologia
Receptor fas/genética
Receptor fas/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD2 Antigens); 0 (CD3 Complex); 0 (CD4 Antigens); 0 (FAS protein, human); 0 (Glucocorticoids); 0 (HLA-DR Antigens); 0 (Interleukin-17); 0 (Interleukin-2); 0 (Interleukins); 0 (Tumor Necrosis Factor-alpha); 0 (fas Receptor); 0 (interleukin-21); EC 3.1.3.48 (Leukocyte Common Antigens); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176303255


  2 / 1967 MEDLINE  
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[PMID]:28525335
[Au] Autor:Balan BJ; Skopinska-Rózewska E; Skopinski P; Zdanowski R; Lesniak M; Kiepura A; Lewicki S
[Ad] Endereço:.
[Ti] Título:Morphometric abnormalities in the spleen of the progeny of mice fed epigallocatechin during gestation and nursing.
[So] Source:Pol J Vet Sci;20(1):5-12, 2017 Mar 28.
[Is] ISSN:1505-1773
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:It is very difficult to cure pregnant females suffering from infections, because of the risk which might occur during treatment by several, even herbal, medications. Many of these substances, among them extracts from plants, have antimicrobial, anti-inflammatory and immunostimulatory properties owing to their polyphenols content, but also may reveal unwanted effects on the fetal development because of their anti-angiogenic properties. The aim of the present study was to elucidate whether daily feeding pregnant and nursing mice 0.2 mg/kg epigallocatechin (EGC), previously recognized as angiogenesis inhibitor, may lead to abnormalities in morphology of spleen and in some parameters of immune function of their adult, 6-week old progeny. Morphometry of EGC offspring spleens revealed lower number of lymphatic nodules and their larger diameter than those found in the control offspring. Cellularity of spleens was lower in EGC offspring than in the controls. Cytometric analysis showed that this decline concerns lymphocytes with CD335 (p<0.001), CD19 (p<0.01) and CD4 (p<0.05) markers. No differences were observed in the humoral response to the immunization with SRBC, and in the proliferative response of splenocytes to mitogens PHA, ConA and LPS.
[Mh] Termos MeSH primário: Catequina/análogos & derivados
Baço/efeitos dos fármacos
Baço/patologia
[Mh] Termos MeSH secundário: Anormalidades Induzidas por Medicamentos
Animais
Animais Recém-Nascidos
Animais Lactentes
Antígenos CD2/imunologia
Catequina/toxicidade
Eritrócitos/metabolismo
Feminino
Lactação
Camundongos
Camundongos Endogâmicos BALB C
Gravidez
Complicações na Gravidez
Ovinos/sangue
Baço/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD2 Antigens); 7Z197MG6QL (gallocatechol); 8R1V1STN48 (Catechin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170520
[St] Status:MEDLINE


  3 / 1967 MEDLINE  
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[PMID]:28237809
[Au] Autor:Kodama S; Shimura T; Kuribayashi H; Abe T; Yoshinari K
[Ad] Endereço:Division of Drug Metabolism and Molecular Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3 Aramaki-Aoba, Aoba-ku, Sendai, Miyagi 980-8578, Japan; Laboratory of Pharmacotherapy of Life-Style Diseases, Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3 Ara
[Ti] Título:Pregnenolone 16α-carbonitrile ameliorates concanavalin A-induced liver injury in mice independent of the nuclear receptor PXR activation.
[So] Source:Toxicol Lett;271:58-65, 2017 Apr 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The pregnane X receptor (PXR) is well-known as a key regulator of drug/xenobiotic clearance. Upon activation by ligand, PXR transcriptionally upregulates the expression of drug-metabolizing enzymes and drug transporters. Recent studies have revealed that PXR also plays a role in regulating immune/inflammatory responses. Specific PXR activators, including synthetic ligands and phytochemicals, have been shown to ameliorate chemically induced colitis in mice. In this study, we investigated an anti-inflammatory effect of pregnenolone 16α-carbonitrile (PCN), a prototypical activator for rodent PXR, in concanavalin A (Con A)-induced liver injury, a model of immune-mediated liver injury, using wild-type and Pxr mice. Unexpectedly, pretreatment with PCN significantly ameliorated Con A-induced liver injury in not only wild-type but Pxr mice as well, accompanied with lowered plasma ALT levels and histological improvements. Pretreatment with PCN was found to significantly repress the induction of Cxcl2 and Ccl2 mRNA expression and neutrophil infiltration into the liver of both wild-type and Pxr mice at the early time point of Con A-induced liver injury. Our results indicate that PCN has unexpected immunosuppressive activity independent of PXR activation to protect mice from immune-mediated liver injury induced by Con A.
[Mh] Termos MeSH primário: Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Concanavalina A
Imunossupressores/farmacologia
Fígado/efeitos dos fármacos
Carbonitrila de Pregnenolona/farmacologia
Receptores de Esteroides/agonistas
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Biomarcadores/sangue
Antígenos CD2/genética
Antígenos CD2/metabolismo
Doença Hepática Induzida por Substâncias e Drogas/sangue
Doença Hepática Induzida por Substâncias e Drogas/genética
Doença Hepática Induzida por Substâncias e Drogas/imunologia
Quimiocina CXCL2/genética
Quimiocina CXCL2/metabolismo
Citoproteção
Modelos Animais de Doenças
Regulação da Expressão Gênica
Fígado/imunologia
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Infiltração de Neutrófilos/efeitos dos fármacos
Receptores de Esteroides/genética
Receptores de Esteroides/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD2 Antigens); 0 (Cd2 protein, rat); 0 (Chemokine CXCL2); 0 (Cxcl2 protein, mouse); 0 (Immunosuppressive Agents); 0 (Receptors, Steroid); 0 (pregnane X receptor); 11028-71-0 (Concanavalin A); 1434-54-4 (Pregnenolone Carbonitrile); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170227
[St] Status:MEDLINE


  4 / 1967 MEDLINE  
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[PMID]:28231026
[Au] Autor:Sridharan V; Seawright JW; Antonawich FJ; Garnett M; Cao M; Singh P; Boerma M
[Ad] Endereço:a University of Arkansas for Medical Sciences, Department of Pharmaceutical Sciences, Division of Radiation Health, Little Rock, Arkansas.
[Ti] Título:Late Administration of a Palladium Lipoic Acid Complex (POLY-MVA) Modifies Cardiac Mitochondria but Not Functional or Structural Manifestations of Radiation-Induced Heart Disease in a Rat Model.
[So] Source:Radiat Res;187(3):361-366, 2017 Mar.
[Is] ISSN:1938-5404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exposure of the heart to ionizing radiation can cause adverse myocardial remodeling. In small animal models, local heart irradiation causes persistent alterations in cardiac mitochondrial function and swelling. POLY-MVA is a dietary supplement that contains a palladium lipoic acid complex that targets mitochondrial complex I and has been demonstrated to have greater redox potential than lipoic acid alone. POLY-MVA improves mitochondrial function and anti-oxidant enzyme activity in the aged rat heart. In this study, we tested whether POLY-MVA can mitigate cardiac effects of ionizing radiation. Adult male rats were exposed to local heart X rays with a daily dose of 9 Gy for 5 consecutive days. Eighteen weeks after irradiation, POLY-MVA was administered orally at 1 ml/kg bodyweight per day during weekdays, for 6 weeks. Alterations in cardiac function as measured with echocardiography coincided with enhanced mitochondrial swelling, a reduction in mitochondrial expression of complex II, manifestations of adverse remodeling such as a reduction in myocardial microvessel density and an increase in collagen deposition and mast cell numbers. POLY-MVA enhanced left ventricular expression of superoxide dismutase 2, but only in sham-irradiated animals. In irradiated animals, POLY-MVA caused a reduction in markers of inflammatory infiltration, CD2 and CD68. Moreover, POLY-MVA mitigated the effects of radiation on mitochondria. Nonetheless, POLY-MVA did not mitigate adverse cardiac remodeling, suggesting that this tissue remodeling may not be alleviated by altering cardiac mitochondria alone. However, we cannot exclude the possibility that an earlier onset of POLY-MVA administration may have more profound effects on radiation-induced cardiac remodeling.
[Mh] Termos MeSH primário: Cardiopatias/patologia
Mitocôndrias Cardíacas/efeitos dos fármacos
Compostos Organometálicos/administração & dosagem
Compostos Organometálicos/farmacologia
Paládio/química
Lesões por Radiação/patologia
Ácido Tióctico/química
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Antígenos de Diferenciação Mielomonocítica/metabolismo
Antígenos CD2/metabolismo
Modelos Animais de Doenças
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/efeitos da radiação
Cardiopatias/metabolismo
Cardiopatias/fisiopatologia
Ventrículos do Coração/efeitos dos fármacos
Ventrículos do Coração/metabolismo
Ventrículos do Coração/efeitos da radiação
Masculino
Mitocôndrias Cardíacas/metabolismo
Lesões por Radiação/metabolismo
Lesões por Radiação/fisiopatologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD2 Antigens); 0 (CD68 antigen, human); 0 (Organometallic Compounds); 5TWQ1V240M (Palladium); 73Y7P0K73Y (Thioctic Acid)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170224
[St] Status:MEDLINE
[do] DOI:10.1667/RR14643.1


  5 / 1967 MEDLINE  
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[PMID]:28063176
[Au] Autor:Hamilton CA; Mahan S; Bell CR; Villarreal-Ramos B; Charleston B; Entrican G; Hope JC
[Ad] Endereço:The Roslin Institute, University of Edinburgh, Midlothian, UK.
[Ti] Título:Frequency and phenotype of natural killer cells and natural killer cell subsets in bovine lymphoid compartments and blood.
[So] Source:Immunology;151(1):89-97, 2017 May.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are widely distributed in lymphoid and non-lymphoid tissues, but little is known about the recirculation of NK cells between blood and tissues. This is relevant to understanding recirculation in the steady-state and also for determining the roles for NK cells in vaccine-induced immunity and responses to infection. Therefore, the percentage of NK cells and their phenotype across peripheral blood, afferent lymph and lymph nodes in steady-state conditions was investigated in cattle using the pseudo-afferent lymphatic cannulation model. CD2 CD25 NK cells were the predominant subset of NK cells within the blood. In contrast, CD2 CD25 NK cells were the main subset present within the skin-draining afferent lymphatic vessels and lymph nodes, indicating that CD2 NK cells are the principal NK cell subset trafficking to lymph nodes via the afferent lymphatic vessel. Furthermore, a low percentage of NK cells were present in efferent lymph, which were predominantly of the CD2 subset, indicating that NK cells can egress from lymph nodes and return to circulation in steady-state conditions. These compartmentalization data indicate that NK cells represent a population of recirculating lymphocytes in steady-state conditions and therefore may be important during immune responses to vaccination or infection.
[Mh] Termos MeSH primário: Células Sanguíneas/imunologia
Bovinos/imunologia
Células Matadoras Naturais/imunologia
Linfonodos/imunologia
Subpopulações de Linfócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD2/metabolismo
Cateterismo
Movimento Celular
Células Cultivadas
Citotoxicidade Imunológica
Imunofenotipagem
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD2 Antigens); 0 (Interleukin-2 Receptor alpha Subunit)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12708


  6 / 1967 MEDLINE  
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[PMID]:27510692
[Au] Autor:Rabade N; Tembhare P; Patkar N; Amare P; Arora B; Subramanian PG; Gujral S
[Ad] Endereço:Department of Pathology, Hematopathology Laboratory, Tata Memorial Hospital, Mumbai, Maharashtra, India.
[Ti] Título:'Childhood systemic mastocytosis associated with t (8; 21) (q22; q22) acute myeloid leukemia'.
[So] Source:Indian J Pathol Microbiol;59(3):407-9, 2016 Jul-Sep.
[Is] ISSN:0974-5130
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:Systemic mastocytosis (SM) with associated clonal nonmast cell lineage disease is seen in up to 20% cases of SM. SM is uncommon in the pediatric population. T (8; 21) (q22; q22) is a good prognostic factor in acute myeloid leukemia (AML). However, the presence of SM confers poor prognosis in t (8; 21) (q22; q22) associated AML. We report the case of a child with t (8; 21) (q22; q22) associated AML with SM and her minimal residual disease status over the course of her treatment. In our case, the abnormal mast cells, showing co-expression of CD25 and CD2, persisted even after the marrow showed no evidence of residual AML.
[Mh] Termos MeSH primário: Leucemia Mieloide Aguda/complicações
Leucemia Mieloide Aguda/diagnóstico
Mastocitose Sistêmica/complicações
Mastocitose Sistêmica/diagnóstico
Translocação Genética
[Mh] Termos MeSH secundário: Medula Óssea/patologia
Antígenos CD2/análise
Criança
Feminino
Seres Humanos
Subunidade alfa de Receptor de Interleucina-2/análise
Mastócitos/química
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (CD2 Antigens); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160812
[St] Status:MEDLINE
[do] DOI:10.4103/0377-4929.188140


  7 / 1967 MEDLINE  
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[PMID]:27469079
[Au] Autor:Rölle A; Halenius A; Ewen EM; Cerwenka A; Hengel H; Momburg F
[Ad] Endereço:Clinical Cooperation Unit Applied Tumor Immunity, Antigen Presentation & T/NK Cell Activation Group, German Cancer Research Center (DKFZ/D121), Heidelberg, Germany. a.roelle@dkfz.de.
[Ti] Título:CD2-CD58 interactions are pivotal for the activation and function of adaptive natural killer cells in human cytomegalovirus infection.
[So] Source:Eur J Immunol;46(10):2420-2425, 2016 Oct.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The existence and expansion of adaptive NK-cell subsets have been linked to HCMV infection. Phenotypically, a majority of adaptive NK cells expresses the activating receptor NKG2C and CD57. Some of the molecular factors driving the expansion of NKG2C CD57 NK cells in HCMV infection have been identified. The direct interaction of adaptive NK cells with HCMV-infected cells, preceding the expansion, however, remains less studied. Recently, adaptive NK cells were reported to express higher levels of the co-activating receptor CD2. We explored whether CD2 was directly involved in the response of adaptive NK cells to HCMV. In a co-culture system of human PBMCs and productively infected fibroblasts, we observed an upregulation of CD69, CD25, and HLA-DR on all NK cells. However, only in adaptive NK cells was this increase largely blocked by antibodies against CD2 and CD58. Functionally, this blockade also resulted in diminished production of IFN-γ and TNF-α by adaptive human NK cells in response to HCMV-infected cells. Our results demonstrate that binding of CD2 to upregulated CD58 on infected cells is a critical event for antibody-mediated activation and subsequent effector functions of adaptive NKG2C CD57 NK cells during the antiviral response.
[Mh] Termos MeSH primário: Antígenos CD2/metabolismo
Antígenos CD58/metabolismo
Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Fibroblastos/imunologia
Células Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Anticorpos/metabolismo
Proliferação Celular
Células Cultivadas
Fibroblastos/virologia
Seres Humanos
Interferon gama/metabolismo
Ativação Linfocitária
Ligação Proteica
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD2 Antigens); 0 (CD58 Antigens); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160730
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646492


  8 / 1967 MEDLINE  
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[PMID]:27385538
[Au] Autor:Koumakis E; Bouaziz M; Dieudé P; Cauvet A; Ruiz B; Airò P; Cusi D; Matucci-Cerinic M; Salvi E; Cuomo G; Hachulla E; Diot E; Caramaschi P; Riccieri V; Avouac J; Allanore Y
[Ad] Endereço:INSERM, Institut Cochin, INSERM U1016, Sorbonne Paris Cité, and Paris Descartes University, Paris; and Paris Descartes University, Rheumatology A Department, Cochin Hospital, APHP, Paris, France.
[Ti] Título:A candidate gene study identifies a haplotype of CD2 as novel susceptibility factor for systemic sclerosis.
[So] Source:Clin Exp Rheumatol;34 Suppl 100(5):43-48, 2016 Sep-Oct.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Systemic sclerosis (SSc) is a rare autoimmune disease (AID) with a complex genetic etiology. Evidence for a shared pathogenesis across AIDs is given by the well-known pleiotropism of autoimmune genes. Recently, several unbiased approaches have identified an association between polymorphisms of the CD2 gene, and rheumatoid arthritis (RA) susceptibility. The objective of this study was to investigate whether CD2 polymorphisms are associated with SSc. METHODS: Two SNPs of CD2, rs624988 and rs798036, were genotyped in a total of 1,786 SSc patients and 2,360 healthy individuals from two European populations (France and Italy). Meta-analyses were performed to assess whether an association exists between CD2 polymorphisms or haplotypes and SSc or its main subtypes. RESULTS: The combined analyses revealed an association between the rs624988 A allele and SSc susceptibility: padj=0.023, OR=1.14 (95%CI 1.04-1.25). Single marker analysis did not reveal any association between rs798036 and SSc. Haplotype analysis identified that the A-T haplotype, previously described in RA, was associated with higher susceptibility for SSc (padj=0.029, OR=1.14, 95%CI 1.04-1.25) and with the positive anti-centromere antibody sub-group of SSc patients (padj=0.009, OR=1.19 95%CI 1.07-1.32). Genotype-mRNA expression correlations revealed that the CD2 risk haplotype was associated with decreased CD2 mRNA expression in SSc patients. CONCLUSIONS: Our study establishes CD2 as a new susceptibility factor for SSc, in a European Caucasian population, confirming the sharing of autoimmune risk factors by SSc and RA.
[Mh] Termos MeSH primário: Autoimunidade/genética
Antígenos CD2/genética
Haplótipos
Polimorfismo de Nucleotídeo Único
Escleroderma Sistêmico/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD2/imunologia
Estudos de Casos e Controles
Grupo com Ancestrais do Continente Europeu/genética
Feminino
França/epidemiologia
Frequência do Gene
Estudos de Associação Genética
Marcadores Genéticos
Predisposição Genética para Doença
Seres Humanos
Itália/epidemiologia
Masculino
Meia-Idade
Razão de Chances
Fenótipo
Fatores de Risco
Escleroderma Sistêmico/diagnóstico
Escleroderma Sistêmico/etnologia
Escleroderma Sistêmico/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; MULTICENTER STUDY
[Nm] Nome de substância:
0 (CD2 Antigens); 0 (Genetic Markers)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE


  9 / 1967 MEDLINE  
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[PMID]:27337048
[Au] Autor:Sable R; Durek T; Taneja V; Craik DJ; Pallerla S; Gauthier T; Jois S
[Ad] Endereço:Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe , Monroe, Louisiana 71201, United States.
[Ti] Título:Constrained Cyclic Peptides as Immunomodulatory Inhibitors of the CD2:CD58 Protein-Protein Interaction.
[So] Source:ACS Chem Biol;11(8):2366-74, 2016 Aug 19.
[Is] ISSN:1554-8937
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interaction between the cell-cell adhesion proteins CD2 and CD58 plays a crucial role in lymphocyte recruitment to inflammatory sites, and inhibitors of this interaction have potential as immunomodulatory drugs in autoimmune diseases. Peptides from the CD2 adhesion domain were designed to inhibit CD2:CD58 interactions. To improve the stability of the peptides, ß-sheet epitopes from the CD2 region implicated in CD58 recognition were grafted into the cyclic peptide frameworks of sunflower trypsin inhibitor and rhesus theta defensin. The designed multicyclic peptides were evaluated for their ability to modulate cell-cell interactions in three different cell adhesion assays, with one candidate, SFTI-a, showing potent activity in the nanomolar range (IC50: 51 nM). This peptide also suppresses the immune responses in T cells obtained from mice that exhibit the autoimmune disease rheumatoid arthritis. SFTI-a was resistant to thermal denaturation, as judged by circular dichroism spectroscopy and mass spectrometry, and had a half-life of ∼24 h in human serum. Binding of this peptide to CD58 was predicted by molecular docking studies and experimentally confirmed by surface plasmon resonance experiments. Our results suggest that cyclic peptides from natural sources are promising scaffolds for modulating protein-protein interactions that are typically difficult to target with small-molecule compounds.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Antígenos CD2/metabolismo
Antígenos CD58/metabolismo
Peptídeos Cíclicos/farmacologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Dicroísmo Circular
Seres Humanos
Espectrometria de Massas
Camundongos
Modelos Moleculares
Ressonância Magnética Nuclear Biomolecular
Peptídeos Cíclicos/química
Ligação Proteica
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (CD2 Antigens); 0 (CD58 Antigens); 0 (Peptides, Cyclic)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160624
[St] Status:MEDLINE
[do] DOI:10.1021/acschembio.6b00486


  10 / 1967 MEDLINE  
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[PMID]:27179621
[Au] Autor:Wagner JA; Fehniger TA
[Ad] Endereço:Department of Medicine, Division of Oncology, Washington University School of Medicine.
[Ti] Título:Human Adaptive Natural Killer Cells: Beyond NKG2C.
[So] Source:Trends Immunol;37(6):351-3, 2016 Jun.
[Is] ISSN:1471-4981
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Paradigm-shifting studies have identified NKG2C(+) adaptive natural killer (NK) cells in individuals infected with cytomegalovirus. Recently in Cell Reports, Liu et al. demonstrate that NKG2C(-/-) HCMV(+) individuals also generate adaptive NK cells, and reveal CD2 as a major co-stimulatory receptor for these NK cells specialized to respond via FcγRIIIa/CD16.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Antígenos CD2/metabolismo
Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Células Matadoras Naturais/imunologia
Subfamília C de Receptores Semelhantes a Lectina de Células NK/metabolismo
Receptores de IgG/metabolismo
[Mh] Termos MeSH secundário: Seres Humanos
Imunidade Inata
Memória Imunológica
Interleucina-12/metabolismo
Interleucina-15/metabolismo
Interleucina-18/metabolismo
Ativação Linfocitária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD2 Antigens); 0 (FCGR3A protein, human); 0 (Interleukin-15); 0 (Interleukin-18); 0 (KLRC2 protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily C); 0 (Receptors, IgG); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160516
[St] Status:MEDLINE



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