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[PMID]:28456791
[Au] Autor:Dondero A; Casu B; Bellora F; Vacca A; De Luisi A; Frassanito MA; Cantoni C; Gaggero S; Olive D; Moretta A; Bottino C; Castriconi R
[Ad] Endereço:Department of Experimental Medicine (DIMES), University of Genova, 16132 Genova, Italy.
[Ti] Título:NK cells and multiple myeloma-associated endothelial cells: molecular interactions and influence of IL-27.
[So] Source:Oncotarget;8(21):35088-35102, 2017 May 23.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiogenesis represents a hallmark of tumor progression in Multiple Myeloma (MM), a still incurable malignancy. Here we analyzed the activity of cytokine-stimulated NK cells against tumor-associated endothelial cells isolated from bone marrow aspirates of MM patients with active disease (MMECs). We show that NK cells activated with optimal doses of IL-15 killed MMECs thanks to the concerted action of multiple activating receptors. In particular, according to the high expression of PVR and Nectin-2 on MMECs, DNAM-1 actively participated in target recognition. Interestingly, in MMECs the surface density of PVR was significantly higher than that detected in endothelium from patients with MM in complete remission or with monoclonal gammopathy of undetermined significance (MGUS). Importantly, IL-27, which unlike IL-15 does not display pro-angiogenic properties, maintained or increased the NK cell functions induced by suboptimal concentrations of IL-15. NK cell properties included killing of MMECs, IFN-γ production as well as a peculiar increase of NKp46 expression on NK cell surface. Finally, IL-27 showed a striking capability of up-regulating the expression of PD-L2 and HLA-I on tumor endothelium, whereas it did not modify that of PD-L1 and HLA-II.Our results suggest that cytokine-activated endogenous or adoptively transferred NK cells might support conventional therapies improving the outcome of MM patients.
[Mh] Termos MeSH primário: Células Endoteliais/efeitos dos fármacos
Interleucinas/metabolismo
Células Matadoras Naturais/efeitos dos fármacos
Mieloma Múltiplo/imunologia
[Mh] Termos MeSH secundário: Idoso
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Feminino
Seres Humanos
Interleucina-15/farmacologia
Células Matadoras Naturais/citologia
Células Matadoras Naturais/metabolismo
Masculino
Meia-Idade
Mieloma Múltiplo/metabolismo
Neovascularização Patológica
Receptores Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL27 protein, human); 0 (Interleukin-15); 0 (Interleukins); 0 (Receptors, Virus); 0 (poliovirus receptor)
[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:170501
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.17070


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[PMID]:29226797
[Au] Autor:Neelapu SS; Locke FL; Bartlett NL; Lekakis LJ; Miklos DB; Jacobson CA; Braunschweig I; Oluwole OO; Siddiqi T; Lin Y; Timmerman JM; Stiff PJ; Friedberg JW; Flinn IW; Goy A; Hill BT; Smith MR; Deol A; Farooq U; McSweeney P; Munoz J; Avivi I; Castro JE; Westin JR; Chavez JC; Ghobadi A; Komanduri KV; Levy R; Jacobsen ED; Witzig TE; Reagan P; Bot A; Rossi J; Navale L; Jiang Y; Aycock J; Elias M; Chang D; Wiezorek J; Go WY
[Ad] Endereço:From the University of Texas M.D. Anderson Cancer Center, Houston (S.S.N., J.R.W.); H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL (F.L.L., J.C.C.); Washington University and Siteman Cancer Center, St. Louis (N.L.B., A. Ghobadi); University of Miami, Miami (L.J.L., K.V.K.); Stanford
[Ti] Título:Axicabtagene Ciloleucel CAR T-Cell Therapy in Refractory Large B-Cell Lymphoma.
[So] Source:N Engl J Med;377(26):2531-2544, 2017 12 28.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In a phase 1 trial, axicabtagene ciloleucel (axi-cel), an autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy, showed efficacy in patients with refractory large B-cell lymphoma after the failure of conventional therapy. METHODS: In this multicenter, phase 2 trial, we enrolled 111 patients with diffuse large B-cell lymphoma, primary mediastinal B-cell lymphoma, or transformed follicular lymphoma who had refractory disease despite undergoing recommended prior therapy. Patients received a target dose of 2×10 anti-CD19 CAR T cells per kilogram of body weight after receiving a conditioning regimen of low-dose cyclophosphamide and fludarabine. The primary end point was the rate of objective response (calculated as the combined rates of complete response and partial response). Secondary end points included overall survival, safety, and biomarker assessments. RESULTS: Among the 111 patients who were enrolled, axi-cel was successfully manufactured for 110 (99%) and administered to 101 (91%). The objective response rate was 82%, and the complete response rate was 54%.With a median follow-up of 15.4 months, 42% of the patients continued to have a response, with 40% continuing to have a complete response. The overall rate of survival at 18 months was 52%. The most common adverse events of grade 3 or higher during treatment were neutropenia (in 78% of the patients), anemia (in 43%), and thrombocytopenia (in 38%). Grade 3 or higher cytokine release syndrome and neurologic events occurred in 13% and 28% of the patients, respectively. Three of the patients died during treatment. Higher CAR T-cell levels in blood were associated with response. CONCLUSIONS: In this multicenter study, patients with refractory large B-cell lymphoma who received CAR T-cell therapy with axi-cel had high levels of durable response, with a safety profile that included myelosuppression, the cytokine release syndrome, and neurologic events. (Funded by Kite Pharma and the Leukemia and Lymphoma Society Therapy Acceleration Program; ZUMA-1 ClinicalTrials.gov number, NCT02348216 .).
[Mh] Termos MeSH primário: Imunoterapia Adotiva
Linfoma Difuso de Grandes Células B/terapia
Receptores de Antígenos de Linfócitos T/uso terapêutico
Linfócitos T/transplante
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD19
Biomarcadores/sangue
Intervalo Livre de Doença
Feminino
Seres Humanos
Interleucinas/sangue
Linfoma Difuso de Grandes Células B/mortalidade
Masculino
Meia-Idade
Doenças do Sistema Nervoso/induzido quimicamente
Neutropenia/induzido quimicamente
Receptores de Antígenos de Linfócitos T/sangue
Taxa de Sobrevida
Linfócitos T/imunologia
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (Biomarkers); 0 (Interleukins); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171212
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1707447


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[PMID]:29353040
[Au] Autor:Jung Y; Kim JC; Park NJ; Bong SK; Lee S; Jegal H; Jin LT; Kim SM; Kim YK; Kim SN
[Ad] Endereço:Natural Products Research Institute, Korea Institute of Science and Technology, Gangneung, Gangwon-do 25451, Republic of Korea.
[Ti] Título:Eupatilin, an activator of PPARα, inhibits the development of oxazolone-induced atopic dermatitis symptoms in Balb/c mice.
[So] Source:Biochem Biophys Res Commun;496(2):508-514, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Eupatilin (5,7-dihydroxy-3',4',6-trimethoxyflavone) is the main lipophilic flavonoid obtained from the Artemisia species. Eupatilin has been reported to have anti-apoptotic, anti-oxidative and anti-inflammatory activities. Previously, we found that eupatilin increases transcriptional activity and expression of peroxisome proliferator-activated receptor α (PPARα) in a keratinocyte cell line and acts as an agonist of PPARα. PPARα agonists ameliorate atopic dermatitis (AD) and restore the skin barrier function. In this study, we confirmed that the effects of eupatilin improved AD-like symptoms in an oxazolone-induced AD-like mouse model. Furthermore, we found that eupatilin suppressed the levels of serum immunoglobulin E (IgE), interleukin-4 (IL-4), and AD involved cytokines, such as tumor necrosis factor α (TNFα), interferon-γ (IFN-γ), IL-1ß, and thymic stromal lymphopoietin (TSLP), IL-33, IL-25 and increased the levels of filaggrin and loricrin in the oxazolone-induced AD-like mouse model. Taken together, our data suggest that eupatilin is a potential candidate for the treatment of AD.
[Mh] Termos MeSH primário: Dermatite Atópica/tratamento farmacológico
Fármacos Dermatológicos/farmacologia
Medicamentos de Ervas Chinesas/farmacologia
Flavonoides/farmacologia
PPAR alfa/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Citocinas/genética
Citocinas/imunologia
Dermatite Atópica/induzido quimicamente
Dermatite Atópica/imunologia
Dermatite Atópica/patologia
Relação Dose-Resposta a Droga
Feminino
Regulação da Expressão Gênica
Imunoglobulina E/sangue
Imunoglobulina E/genética
Interferon gama/genética
Interferon gama/imunologia
Interleucina-1beta/genética
Interleucina-1beta/imunologia
Interleucina-33/genética
Interleucina-33/imunologia
Interleucina-4/genética
Interleucina-4/imunologia
Interleucinas/genética
Interleucinas/imunologia
Proteínas de Filamentos Intermediários/genética
Proteínas de Filamentos Intermediários/imunologia
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Oxazolona
PPAR alfa/imunologia
Ratos
Transdução de Sinais
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (D17Wsu104e protein, mouse); 0 (Dermatologic Agents); 0 (Drugs, Chinese Herbal); 0 (Flavonoids); 0 (IL1B protein, mouse); 0 (Il33 protein, mouse); 0 (Interleukin-1beta); 0 (Interleukin-33); 0 (Interleukins); 0 (Intermediate Filament Proteins); 0 (Membrane Proteins); 0 (PPAR alpha); 0 (Tumor Necrosis Factor-alpha); 0 (filaggrin); 0 (loricrin); 0 (thymic stromal lymphopoietin); 15646-46-5 (Oxazolone); 207137-56-2 (Interleukin-4); 37341-29-0 (Immunoglobulin E); 4D58O05490 (eupatilin); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


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[PMID]:28461110
[Au] Autor:Zhu J; Zeng Y; Dolff S; Bienholz A; Lindemann M; Brinkhoff A; Schedlowski M; Xu S; Sun M; Guberina H; Kirchhof J; Kribben A; Witzke O; Wilde B
[Ad] Endereço:Department of Nephrology, University Hospital Essen, University Duisburg-Essen, Hufelandstr. 55, 45147 Essen, Germany.
[Ti] Título:Granzyme B producing B-cells in renal transplant patients.
[So] Source:Clin Immunol;184:48-53, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: A separate subset of Granzyme B (GrB) producing B-cells regulating T-cell mediated immunity has been identified. In the present study, we investigated the role of GrB B-cells in renal transplant patients (RTX). METHODS: 12 healthy controls (HC) and 26 RTX patients were enrolled. In addition, 19 healthy volunteers treated with cyclosporine A (CsA) were enrolled. GrB B-cells were determined via flow cytometry. RESULTS: RTX Patients showed a diminished fraction of GrB B-cells as compared to HC. CsA treatment of healthy volunteers had no impact on the development of GrB B-cells. RTX patients with a history of allograft rejection showed an increased frequency of GrB B-cells. RTX patients with at least one episode of CMV viremia tended to have lower GrB B-cells as compared to patients without viremic episodes. CONCLUSION: We demonstrate that treatment with CsA does not impair the development of GrB B-cells. GrB B-cells may have a dual role in renal transplantation as regulatory cells to maintain allospecific tolerance and as effector cells enhancing viral control.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Granzimas/metabolismo
Transplante de Rim
[Mh] Termos MeSH secundário: Corticosteroides/uso terapêutico
Idoso
Linfócitos B/efeitos dos fármacos
Estudos de Casos e Controles
Ciclosporina/farmacologia
Ciclosporina/uso terapêutico
Feminino
Rejeição de Enxerto/prevenção & controle
Granzimas/efeitos dos fármacos
Seres Humanos
Imunossupressores/farmacologia
Imunossupressores/uso terapêutico
Interleucinas/farmacologia
Masculino
Meia-Idade
Ácido Micofenólico/uso terapêutico
Tacrolimo/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Immunosuppressive Agents); 0 (Interleukins); 0 (interleukin-21); 83HN0GTJ6D (Cyclosporine); EC 3.4.21.- (GZMB protein, human); EC 3.4.21.- (Granzymes); HU9DX48N0T (Mycophenolic Acid); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:27774606
[Au] Autor:Vallières F; Girard D
[Ad] Endereço:Laboratoire de recherche en inflammation et physiologie des granulocytes, Université du Québec, INRS-Institut Armand-Frappier, Laval, QC, Canada.
[Ti] Título:Mechanism involved in interleukin-21-induced phagocytosis in human monocytes and macrophages.
[So] Source:Clin Exp Immunol;187(2):294-303, 2017 Feb.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The interleukin (IL)-21/IL-21 receptor (R) is a promising system to be exploited for the development of therapeutic strategies. Although the biological activities of IL-21 and its cell signalling events have been largely studied in immunocytes, its interaction with human monocytes and macrophages have been neglected. Previously, we reported that IL-21 enhances Fc gamma receptor (FcRγ)-mediated phagocytosis in human monocytes and in human monocyte-derived macrophages (HMDM) and identified Syk as a novel molecular target of IL-21. Here, we elucidate further how IL-21 promotes phagocytosis in these cells. Unlike its ability to enhance phagocytosis of opsonized sheep red blood cells (SRBCs), IL-21 did not promote phagocytosis of Escherichia coli and zymosan by monocytes and did not alter the cell surface expression of CD16, CD32 and CD64. In HMDM, IL-21 was found to enhance phagocytosis of zymosan. In addition, we found that IL-21 activates p38, protein kinase B (Akt), signal transducer and activator of transcription (STAT)-1 and STAT-3 in monocytes and HMDM. Using a pharmacological approach, we demonstrate that IL-21 enhances phagocytosis by activating some mitogen-activated protein kinases (MAPKs) and phosphoinositide 3-kinase (PI3K)-Akt and Janus kinase (JAK)-STAT pathways. These results obtained in human monocytes and macrophages have to be considered for a better exploitation of the IL-21/IL-21R system for therapeutic purposes.
[Mh] Termos MeSH primário: Escherichia coli/imunologia
Interleucinas/metabolismo
Macrófagos/imunologia
Fagocitose
Receptores de Interleucina-21/metabolismo
[Mh] Termos MeSH secundário: Animais
Bovinos
Células Cultivadas
Eritrócitos/imunologia
Seres Humanos
Interleucinas/imunologia
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Zimosan/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukins); 0 (Receptors, Interleukin-21); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (interleukin-21); 9010-72-4 (Zymosan); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12886


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[PMID]:28747343
[Au] Autor:Savage AK; Liang HE; Locksley RM
[Ad] Endereço:Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158.
[Ti] Título:The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine.
[So] Source:J Immunol;199(5):1912-1922, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group 3 innate lymphoid cells (ILC3s) are important for intestinal health, particularly in controlling inflammation in response to epithelial dysregulation, but their role during homeostasis remains less well understood. We generated IL-22 reporter mice to assess production of this key cytokine by ILC3s in the small intestine during development and under basal conditions. Although IL-22 is produced by a variety of lymphocyte populations, constitutively high IL-22 expression was limited to lymphoid-tissue inducer (LTi) cells residing in lymph node-like structures in the gut called solitary intestinal lymphoid tissues (SILT). Constitutive IL-22 expression was dependent on the microbiota and MyD88 signaling, appeared upon weaning, and was present across the spectrum of SILT, including in cryptopatches. Activated SILT LTi cells colocalized with a rare subpopulation of activated macrophages constitutively positive for IL-12/23 p40 and capable of activating neonatal LTi cells in response to TLR stimulus. Thus, weaning leads to the organization of innate immune activation hubs at SILT that mature and are continuously sustained by signals from the microbiota. This functional and anatomic organization constitutes a significant portion of the steady-state IL-23/IL-22 axis.
[Mh] Termos MeSH primário: Interleucinas/metabolismo
Intestino Delgado/imunologia
Linfócitos/imunologia
Macrófagos/imunologia
Estruturas Linfoides Terciárias/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Imunidade Inata
Interleucina-12/metabolismo
Interleucina-23/metabolismo
Interleucinas/genética
Intestino Delgado/anatomia & histologia
Ativação Linfocitária
Linfócitos/citologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microbiota/imunologia
Fator 88 de Diferenciação Mieloide/metabolismo
Transdução de Sinais
Estruturas Linfoides Terciárias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-23); 0 (Interleukins); 0 (Myd88 protein, mouse); 0 (Myeloid Differentiation Factor 88); 0 (interleukin-22); 187348-17-0 (Interleukin-12)
[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.1700155


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[PMID]:28468967
[Au] Autor:Keller B; Stumpf I; Strohmeier V; Usadel S; Verhoeyen E; Eibel H; Warnatz K
[Ad] Endereço:Center for Chronic Immunodeficiency, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
[Ti] Título:High SYK Expression Drives Constitutive Activation of CD21 B Cells.
[So] Source:J Immunol;198(11):4285-4292, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human CD21 B cells present with an activated phenotype and accumulate in distinct disorders connected with chronic immune stimulation. Signaling studies had revealed an increased basal phosphorylation of spleen tyrosine kinase (SYK) and phospholipase Cγ2. Additional BCR stimulation of these constitutively active cells, however, led to reduced activation of these signaling molecules and subsequently NF-κB and Ca activation. In this article, we demonstrate that high SYK expression is a common feature of CD21 B cells independent of the underlying disorder, and that this high expression is sufficient to drive constitutive phosphorylation of SYK and its immediate targets Bruton's tyrosine kinase and phospholipase Cγ2. Inhibition of SYK activity eliminated features of the constitutive activation in these cells and partly restored BCR signaling. High SYK expression is especially induced by CpG or CD40L in combination with IL-21, but not BCR stimulation, suggesting the importance of the immune-stimulatory context for the induction of this B cell phenotype. In summary, high SYK expression is a common feature of human CD21 B cells and presumably results from chronic activation in inflammatory environments present in a subgroup of patients with heterogeneous disorders like chronic infection, autoimmunity, and immunodeficiency. High SYK expression by itself drives the constitutive activation observed in these B cells, which in turn may contribute to the hyporesponsiveness upon BCR stimulation. Given the high prevalence of autoreactive clones among CD21 B cells in autoimmune disorders, the dominant role of SYK in CD21 B cells may provide a new option for therapeutic interventions in patients with expanded CD21 B cells and humoral autoimmunity.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Ativação Linfocitária
Receptores de Complemento 3d/imunologia
Quinase Syk/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Linfócitos B/fisiologia
Ligante de CD40/imunologia
Feminino
Seres Humanos
Interleucinas/farmacologia
Masculino
Meia-Idade
Oligodesoxirribonucleotídeos/imunologia
Fosfolipase C gama/metabolismo
Fosforilação
Proteínas Tirosina Quinases/metabolismo
Receptores de Antígenos de Linfócitos B/imunologia
Transdução de Sinais
Quinase Syk/antagonistas & inibidores
Quinase Syk/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CPG-oligonucleotide); 0 (Interleukins); 0 (Oligodeoxyribonucleotides); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Complement 3d); 0 (interleukin-21); 147205-72-9 (CD40 Ligand); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (SYK protein, human); EC 2.7.10.2 (Syk Kinase); EC 3.1.4.3 (Phospholipase C gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700079


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[PMID]:28741298
[Au] Autor:Petta S; Valenti L; Tuttolomondo A; Dongiovanni P; Pipitone RM; Cammà C; Cabibi D; Di Marco V; Fracanzani AL; Badiali S; Nobili V; Fargion S; Grimaudo S; Craxì A
[Ad] Endereço:Sezione di Gastroenterologia e Epatologia, DiBiMIS, University of Palermo, Palermo, Italy.
[Ti] Título:Interferon lambda 4 rs368234815 TT>δG variant is associated with liver damage in patients with nonalcoholic fatty liver disease.
[So] Source:Hepatology;66(6):1885-1893, 2017 12.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interferon (IFN) lambda 3/4 (IFNL3/4) locus, influencing innate immunity regulation, has been associated with the severity of hepatitis and fibrosis progression during chronic hepatitis C infection, while contrasting results were reported in nonalcoholic fatty liver disease. In this study, we examined whether rs12979860 and the linked causal rs368234815 variant encoding for the alternative IFNL4 protein variant are associated with liver fibrosis and damage in a large multicenter cohort of patients at risk of nonalcoholic steatohepatitis. To clarify the mechanism, we also evaluated the impact on IFN-stimulated gene hepatic expression in a subset of patients. We considered 946 consecutive Italian individuals at risk of nonalcoholic steatohepatitis with liver histology evaluated according to Kleiner. The rs368234815 TT>δG, rs12979860 C>T, and patatin-like phospholipase-3 rs738409 C>G polymorphisms were genotyped; and IFN-stimulated gene hepatic expression (n = 16) was tested by TaqMan assays. We found that the rs368234815 TT allele was independently associated with severe F3-F4 fibrosis (odds ratio, 1.53; 95% confidence interval, 1.15-2.31; P = 0.005) and with severe (grade 2-3) lobular necroinflammation (odds ratio, 1.47; 95% confidence interval, 1.14-1.88; P = 0.002). The impact of rs368234815 on liver damage was generally more marked in nonobese individuals, where association with severe fibrosis, necroinflammation, and nonalcoholic steatohepatitis was observed (P < 0.05). IFN-stimulated genes were hypo-expressed in the liver of patients carrying the IFNL4 rs368234815 TT/TT genotype (P < 0.05). Similar results were observed when considering the rs12979860 polymorphism, which was in high linkage disequilibrium with rs368234815 (R = 0.87). CONCLUSION: The IFNL4 genotype is associated with severity of fibrosis in nonalcoholic fatty liver disease patients of European ancestry, likely by modulating the activation of innate immunity and necroinflammation. (Hepatology 2017;66:1885-1893).
[Mh] Termos MeSH primário: Interleucinas/genética
Hepatopatia Gordurosa não Alcoólica/genética
[Mh] Termos MeSH secundário: Adulto
Feminino
Fibrose
Expressão Gênica
Seres Humanos
Fígado/metabolismo
Fígado/patologia
Masculino
Meia-Idade
Hepatopatia Gordurosa não Alcoólica/metabolismo
Hepatopatia Gordurosa não Alcoólica/patologia
Polimorfismo de Nucleotídeo Único
Estudos Prospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IFNL4 protein, human); 0 (Interleukins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29395


  9 / 14269 MEDLINE  
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[PMID]:29186193
[Au] Autor:Sprokholt JK; Kaptein TM; van Hamme JL; Overmars RJ; Gringhuis SI; Geijtenbeek TBH
[Ad] Endereço:Department of Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
[Ti] Título:RIG-I-like receptor activation by dengue virus drives follicular T helper cell formation and antibody production.
[So] Source:PLoS Pathog;13(11):e1006738, 2017 Nov.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Follicular T helper cells (TFH) are fundamental in orchestrating effective antibody-mediated responses critical for immunity against viral infections and effective vaccines. However, it is unclear how virus infection leads to TFH induction. We here show that dengue virus (DENV) infection of human dendritic cells (DCs) drives TFH formation via crosstalk of RIG-I-like receptor (RLR) RIG-I and MDA5 with type I Interferon (IFN) signaling. DENV infection leads to RLR-dependent IKKε activation, which phosphorylates IFNα/ß receptor-induced STAT1 to drive IL-27 production via the transcriptional complex ISGF3. Inhibiting RLR activation as well as neutralizing antibodies against IL-27 prevented TFH formation. DENV-induced CXCR5+PD-1+Bcl-6+ TFH cells secreted IL-21 and activated B cells to produce IgM and IgG. Notably, RLR activation by synthetic ligands also induced IL-27 secretion and TFH polarization. These results identify an innate mechanism by which antibodies develop during viral disease and identify RLR ligands as potent adjuvants for TFH-promoting vaccination strategies.
[Mh] Termos MeSH primário: Anticorpos Antivirais/imunologia
Vírus da Dengue/fisiologia
Dengue/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Mh] Termos MeSH secundário: Formação de Anticorpos
Linfócitos B/imunologia
Proteína DEAD-box 58/genética
Proteína DEAD-box 58/imunologia
Células Dendríticas/imunologia
Dengue/genética
Dengue/virologia
Seres Humanos
Helicase IFIH1 Induzida por Interferon/genética
Helicase IFIH1 Induzida por Interferon/imunologia
Interleucina-27/genética
Interleucina-27/imunologia
Interleucinas/genética
Interleucinas/imunologia
Ativação Linfocitária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Interleukin-27); 0 (Interleukins); 0 (interleukin-21); EC 3.6.1.- (DDX58 protein, human); EC 3.6.1.- (IFIH1 protein, human); EC 3.6.4.13 (DEAD Box Protein 58); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006738


  10 / 14269 MEDLINE  
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[PMID]:29277790
[Au] Autor:Shamoun L; Kolodziej B; Andersson RE; Dimberg J
[Ad] Endereço:Division of Medical Diagnostics, Department of Laboratory Medicine, Jönköping County, Jönköping, Sweden.
[Ti] Título:Protein Expression and Genetic Variation of and Association with Colorectal Cancer in Swedish Patients.
[So] Source:Anticancer Res;38(1):321-328, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Interleukin 32 (IL32) is an intracellular pluripotent cytokine produced by epithelial cells, monocytes, T-lymphocytes and natural killer cells and seems to be involved in the pathogenesis of cancer and inflammatory diseases. Our purpose was to assess the role of protein expression and genetic polymorphisms of IL32 in colorectal cancer (CRC) susceptibility. MATERIALS AND METHODS: To gain insight into clinical significance of IL32 in Swedish patients with CRC, using enzyme-linked immunosorbent assay, we determined whether IL32 protein level is altered in CRC tissue (n=75) compared with paired normal tissue and in plasma from patients with CRC (n=94) compared with controls (n=81). The expression of IL32 protein was confirmed by immunohistochemistry (n=73). We used Luminex technology to investigate protein levels of the cytokines IL6, tumor necrosis factor-α (TNFα) and vascular endothelial growth factor (VEGF) to relate these to IL32 levels in CRC tissue. Three single nucleotide polymorphisms (SNPs) (rs28372698, rs12934561, rs4786370) of the IL32 gene have been proposed as modifiers for different diseases. The present study evaluated the susceptibility of patients possessing these SNPs to CRC. Using TaqMan SNP genotyping assays, these SNPs were screened in Swedish patients with CRC (n=465) and healthy controls (n=331). RESULTS: We found no significant differences in the genotypic frequencies between the patients and healthy controls and no relation to survival for any of the SNPs. However, the SNP rs12934561 was statisticalLY significant associated with older patients. IL32 protein was up-regulated in CRC tissue and related to IL6, TNFα, and VEGF, and seems to be modulated by SNP rs28372698. The IL32 protein level in CRC tissue also reflects both disseminated disease and location. CONCLUSION: Our results suggest that altered IL32 protein concentrations in CRC tissue and genotypic variants of IL32 are related to disseminated CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Detecção Precoce de Câncer/métodos
Predisposição Genética para Doença
Interleucinas/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/metabolismo
Neoplasias Colorretais/patologia
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Interleucina-6/metabolismo
Interleucinas/sangue
Interleucinas/metabolismo
Masculino
Meia-Idade
Suécia
Fator de Necrose Tumoral alfa/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (IL32 protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (Interleukins); 0 (Tumor Necrosis Factor-alpha); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE



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