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[PMID]:27776738
[Au] Autor:Cheng Z; Peng HL; Zhang R; Fu XM; Zhang GS
[Ad] Endereço:Department of Hematology, Institute of Molecular Hematology, The Second Xiang-ya Hospital, Central South University, Changsha, Hunan, PR China.
[Ti] Título:Bone marrow-derived innate macrophages attenuate oxazolone-induced colitis.
[So] Source:Cell Immunol;311:46-53, 2017 Jan.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that a subpopulation of granulocyte macrophage colony-stimulating factor (GM-CSF)-dependent F4/80 CD11b innate macrophages could be derived from bone marrow cells by continuous in vitro culturing. These cells could be induced to differentiate into M1 or M2 macrophages in vitro. In the current study, we sought to determine whether bone marrow cell-derived innate macrophages (BMIMs) could be used to fulfill an anti-inflammatory purpose by intravenous transplantation in vivo after being stimulated to differentiate into M2 macrophages. Because Th2 cytokines, such as interleukin IL-4 and IL-13, can induce macrophage polarization into M2 macrophages, we treated the BMIMs with IL-4 and IL-13 in vitro. Next, the M2 macrophages were intravenously transplanted into a typical Th2-mediated inflammatory disease model, oxazolone (OXZ)-induced colitis, to assess the anti-inflammatory activity of BMIM-derived M2 macrophages (BMIM-M2Ms) in vivo. After transplantation, the severity of intestinal inflammation was attenuated. In addition, colon lengths and mouse body weights were noticeably improved. F4/80 CD206 double-positive cells (displaying the markers of M2 macrophages) had accumulated in the colon tissue of BMIM-M2M-transplanted mice. This evidence demonstrated that bone marrow-derived BMIM-M2Ms could be used to alleviate OXZ-induced Th2-mediated inflammation in a mouse model in vivo.
[Mh] Termos MeSH primário: Colite/imunologia
Colite/terapia
Macrófagos/transplante
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/metabolismo
Antígeno CD11b/metabolismo
Células Cultivadas
Colite/induzido quimicamente
Citocinas/metabolismo
Modelos Animais de Doenças
Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo
Seres Humanos
Imunidade Inata
Lectinas Tipo C/metabolismo
Macrófagos/imunologia
Lectinas de Ligação a Manose/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Oxazolona
Fenótipo
Receptores de Superfície Celular/metabolismo
Células Th2/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (CD11b Antigen); 0 (Cytokines); 0 (Lectins, C-Type); 0 (Mannose-Binding Lectins); 0 (Receptors, Cell Surface); 0 (mannose receptor); 0 (monocyte-macrophage differentiation antigen); 15646-46-5 (Oxazolone); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171217
[Lr] Data última revisão:
171217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:28747319
[Au] Autor:Sudworth A; Vaage JT; Inngjerdingen M; Kveberg L
[Ad] Endereço:Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
[Ti] Título:Frontline Science: A hyporesponsive subset of rat NK cells negative for Ly49s3 and NKR-P1B are precursors to the functionally mature NKR-P1B subset.
[So] Source:J Leukoc Biol;102(6):1289-1298, 2017 Dec.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rat NK cells are divided into major subsets expressing either Ly49 receptors or the inhibitory NKR-P1B receptor in conjunction with NKG2A/C/E receptors. A minor subset of NKp46 cells lacking expression of both Ly49 receptors and NKR-P1B is present in blood and spleen and is associated with decreased functional competence. We hypothesized that this subset may represent precursors to Ly49 and/or NKR-P1B NK cells. When cultured in vitro in IL-2 and IL-15 or adoptively transferred to syngeneic hosts, a portion of NKR-P1B Ly49s3 cells transformed to express NKR-P1B, but very little Ly49s3. Acquisition of NKR-P1B by NKR-P1B Ly49s3 cells coincided with increased degranulation. In addition, although NKR-P1B Ly49s3 cells highly proliferate, proliferative activity was reduced upon acquisition of NKR-P1B at comparable levels to bona fide NKR-P1B NK cells. A fraction of NKR-P1B Ly49s3 cells remained negative for NKR-P1B, both in vitro and after adoptive transfer in vivo. Most NKR-P1B Ly49s3 cells expressed the transcription factor Eomesodermin and NK cell markers, indicating that these cells represent conventional NK cells. Our findings suggest that the NKR-P1B Ly49s3 NK cells are precursors to NKR-P1B single-positive cells and that functional competence is acquired upon expression of NKR-P1B.
[Mh] Termos MeSH primário: Diferenciação Celular
Células Matadoras Naturais/citologia
Células Matadoras Naturais/metabolismo
Subfamília A de Receptores Semelhantes a Lectina de Células NK/metabolismo
Receptores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Antígeno CD11b/metabolismo
Degranulação Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Interleucina-15/farmacologia
Interleucina-2/farmacologia
Células Matadoras Naturais/efeitos dos fármacos
Células Matadoras Naturais/fisiologia
Fenótipo
Ratos
Baço/citologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Ly49s3 protein, rat); 0 (NK Cell Lectin-Like Receptor Subfamily A); 0 (NKR-P1B protein, rat); 0 (Receptors, Immunologic)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.1HI0517-177RR


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[PMID]:29049725
[Au] Autor:Subhi Y; Krogh Nielsen M; Molbech CR; Oishi A; Singh A; Nissen MH; Sørensen TL
[Ad] Endereço:Clinical Eye Research Division, Department of Ophthalmology, Zealand University Hospital, Roskilde, Denmark.
[Ti] Título:CD11b and CD200 on Circulating Monocytes Differentiate Two Angiographic Subtypes of Polypoidal Choroidal Vasculopathy.
[So] Source:Invest Ophthalmol Vis Sci;58(12):5242-5250, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: To investigate surface expression of CD11b and CD200 on circulating monocytes in patients with polypoidal choroidal vasculopathy (PCV). Methods: This was a prospective case-control study of patients with PCV (n = 27), age-matched healthy controls (n = 27), and patients with neovascular AMD (n = 49). All participants underwent a comprehensive ocular examination. Fluorescein and indocyanine green angiography were performed in patients suspected of neovascular AMD or PCV. Polypoidal choroidal vasculopathy was angiographically categorized into those with a strong presence of a branching vascular network (BVN) (type 1) or with a faint/no clear presence of a BVN (type 2). Fresh venous blood was stained with fluorescent antibodies for flow cytometric analyses. We compared the percentages of CD11b+, CD200+, and CD11b+CD200+ monocytes between groups of diagnosis and between different angiographic subtypes of PCV. Results: Overall, CD11b+ monocytes were both increased in patients with PCV and neovascular AMD. CD200+ and CD11b+CD200+ monocytes were increased in patients with neovascular AMD. An age-related increase in CD11b+CD200+ monocytes was absent in patients with PCV and neovascular AMD. Patients with PCV type 1 had significantly higher CD11b+, CD200+, and CD11b+CD200+ monocytes, whereas patients with PCV type 2 had levels similar to that in healthy controls. Conclusions: We found that PCV is immunologically heterogeneous with significant differences between angiographic subtypes. Increased CD11b+ and CD200+ monocytes in those with a strong presence of BVN indicate that BVN development may be associated with retinal injury and a VEGF-mediated process that is either reflected or propelled by systemic changes in monocytes.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Biomarcadores/metabolismo
Antígeno CD11b/metabolismo
Neovascularização de Coroide/sangue
Monócitos/metabolismo
Pólipos/sangue
[Mh] Termos MeSH secundário: Idoso
Estudos de Casos e Controles
Neovascularização de Coroide/diagnóstico
Corantes/administração & dosagem
Feminino
Citometria de Fluxo
Angiofluoresceinografia
Seres Humanos
Verde de Indocianina/administração & dosagem
Degeneração Macular/sangue
Degeneração Macular/diagnóstico
Masculino
Pólipos/diagnóstico
Estudos Prospectivos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Biomarkers); 0 (CD11b Antigen); 0 (Coloring Agents); 0 (ITGAM protein, human); 0 (antigens, CD200); IX6J1063HV (Indocyanine Green)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22479


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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


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[PMID]:28961278
[Au] Autor:McClellan SA; Jerome A; Suvas S; Hazlett LD
[Ad] Endereço:Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States of America.
[Ti] Título:NLRC4 regulates caspase-1 and IL-1beta production in a CD11blowLy6Glow population of cells required for resistance to Pseudomonas aeruginosa keratitis.
[So] Source:PLoS One;12(9):e0185718, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Psbetaeudomonas (P.) aeruginosa infection of the cornea in BALB/c mice does not result in perforation and the mice have been classified as resistant. However, regulation of this response via inflammasome activation remained untested. Therefore, BALB/c mice were infected with P. aeruginosa ATCC strain 19660 and NLRP3 and NLRC4 protein tested by ELISA. Since NLRC4 vs NLRP3 protein levels were significantly higher in the corneas of BALB/c at 1 and 5 days postinfection we used silencing to knockdown NLRC4. Silencing NLRC4 vs scrambled siRNA treatment exacerbated disease in BALB/c mice, reduced myeloperoxidase levels and elevated bacterial plate counts at 5 days postinfection. It also increased pro IL-1beta, but reduced total protein for IL-1beta and IL-18 at 5 days postinfection. Flow cytometry to identify cells affected by silencing, showed reduced caspase-1 levels in a CD11blowLy6Glow population of cells, (but not PMN or macrophages) from the infected cornea of siNLRC4 treated mice that produced less mature IL-1beta. These data provide evidence that the NLRC4 inflammasome contributes to resistance through regulation of caspase-1, IL-1beta and IL-18 in a CD11blowLy6Glow population of cells.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/fisiologia
Antígeno CD11b/imunologia
Proteínas de Ligação ao Cálcio/fisiologia
Caspase 1/biossíntese
Interleucina-1beta/biossíntese
Ceratite/imunologia
Infecções por Pseudomonas/imunologia
Pseudomonas aeruginosa/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/genética
Proteínas de Ligação ao Cálcio/genética
Contagem de Colônia Microbiana
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Técnicas de Silenciamento de Genes
Ceratite/microbiologia
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Pseudomonas/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (CD11b Antigen); 0 (Calcium-Binding Proteins); 0 (Interleukin-1beta); 0 (Ipaf protein, mouse); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185718


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[PMID]:28753653
[Au] Autor:Gabriel TL; Mirzaian M; Hooibrink B; Ottenhoff R; van Roomen C; Aerts JMFG; van Eijk M
[Ad] Endereço:Department of Medical Biochemistry, Academic Medical Center, Amsterdam, The Netherlands.
[Ti] Título:Induction of Sphk1 activity in obese adipose tissue macrophages promotes survival.
[So] Source:PLoS One;12(7):e0182075, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During obesity, adipose tissue macrophages (ATM) are increased in concert with local inflammation and insulin resistance. Since the levels of sphingolipid (SLs) in adipose tissue (AT) are altered during obesity we investigated the potential impact of SLs on ATMs. For this, we first analyzed expression of SL metabolizing genes in ATMs isolated from obese mice. A marked induction of sphingosine kinase 1 (Sphk1) expression was observed in obese ATM when compared to lean ATM. This induction was observed in both MGL-ve (M1) and MGL1+ve (M2) macrophages from obese WAT. Next, RAW264.7 cells were exposed to excessive palmitate, resulting in a similar induction of Sphk1. This Sphk1 induction was also observed when cells were treated with chloroquine, a lysosomotropic amine impacting lysosome function. Simultaneous incubation of RAW cells with palmitate and the Sphk1 inhibitor SK1-I promoted cell death, suggesting a protective role of Sphk1 during lipotoxic conditions. Interestingly, a reduction of endoplasmic reticulum (ER) stress related genes was detected in obese ATM and was found to be associated with elevated Sphk1 expression. Altogether, our data suggest that lipid overload in ATM induces Sphk1, which promotes cell viability.
[Mh] Termos MeSH primário: Tecido Adiposo/citologia
Sobrevivência Celular/fisiologia
Macrófagos/metabolismo
Obesidade/metabolismo
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Cloroquina/farmacologia
Análise por Conglomerados
Dieta Hiperlipídica/efeitos adversos
Macrófagos/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
Ácido Palmítico/farmacologia
Células RAW 264.7
Esfingolipídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Sphingolipids); 2V16EO95H1 (Palmitic Acid); 886U3H6UFF (Chloroquine); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 2.7.1.- (sphingosine kinase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182075


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[PMID]:28732201
[Au] Autor:Chen CC; Butz ES; Chao YK; Grishchuk Y; Becker L; Heller S; Slaugenhaupt SA; Biel M; Wahl-Schott C; Grimm C
[Ad] Endereço:Department of Pharmacy, Center for Drug Research and Center for Integrated Protein Science Munich (CIPSM), Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
[Ti] Título:Small Molecules for Early Endosome-Specific Patch Clamping.
[So] Source:Cell Chem Biol;24(7):907-916.e4, 2017 Jul 20.
[Is] ISSN:2451-9456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To resolve the subcellular distribution of endolysosomal ion channels, we have established a novel experimental approach to selectively patch clamp Rab5 positive early endosomes (EE) versus Rab7/LAMP1-positive late endosomes/lysosomes (LE/LY). To functionally characterize ion channels in endolysosomal membranes with the patch-clamp technique, it is important to develop techniques to selectively enlarge the respective organelles. We found here that two small molecules, wortmannin and latrunculin B, enlarge Rab5-positive EE when combined but not Rab7-, LAMP1-, or Rab11 (RE)-positive vesicles. The two compounds act rapidly, specifically, and are readily applicable in contrast to genetic approaches or previously used compounds such as vacuolin, which enlarges EE, RE, and LE/LY. We apply this approach here to measure currents mediated by TRPML channels, in particular TRPML3, which we found to be functionally active in both EE and LE/LY in overexpressing cells as well as in endogenously expressing CD11b+ lung-tissue macrophages.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Androstadienos/farmacologia
Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia
Endossomos/metabolismo
Tiazolidinas/farmacologia
[Mh] Termos MeSH secundário: Aminopiridinas/farmacologia
Antígeno CD11b/metabolismo
Endossomos/efeitos dos fármacos
Células HEK293
Compostos Heterocíclicos com 3 Anéis/farmacologia
Seres Humanos
Pulmão/citologia
Pulmão/metabolismo
Proteína 1 de Membrana Associada ao Lisossomo/metabolismo
Lisossomos/efeitos dos fármacos
Lisossomos/metabolismo
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Macrófagos Peritoneais/citologia
Macrófagos Peritoneais/efeitos dos fármacos
Macrófagos Peritoneais/metabolismo
Técnicas de Patch-Clamp
Canais de Receptores Transientes de Potencial/genética
Canais de Receptores Transientes de Potencial/metabolismo
Proteínas rab de Ligação ao GTP/metabolismo
Proteínas rab5 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-amino-N-(3-(4-(4-morpholinyl)pyrido(3',2'-4,5)furo(3,2-d)pyrimidin-2-yl)phenyl)-3-pyridinecarboxamide); 0 (Aminopyridines); 0 (Androstadienes); 0 (Bridged Bicyclo Compounds, Heterocyclic); 0 (CD11b Antigen); 0 (Heterocyclic Compounds, 3-Ring); 0 (Lysosomal-Associated Membrane Protein 1); 0 (MCOLN1 protein, human); 0 (MCOLN3 protein, human); 0 (Thiazolidines); 0 (Transient Receptor Potential Channels); 152989-05-4 (rab7 protein); EC 3.6.1.- (rab11 protein); EC 3.6.5.2 (rab GTP-Binding Proteins); EC 3.6.5.2 (rab5 GTP-Binding Proteins); LW7U308U7U (latrunculin B); XVA4O219QW (wortmannin)
[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:170722
[St] Status:MEDLINE


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[PMID]:28710252
[Au] Autor:Collin R; St-Pierre C; Guilbault L; Mullins-Dansereau V; Policheni A; Guimont-Desrochers F; Pelletier AN; Gray DH; Drobetsky E; Perreault C; Hillhouse EE; Lesage S
[Ad] Endereço:Department of Immunology-Oncology, Maisonneuve-Rosemont Hospital, Montreal, Quebec H1T 2M4, Canada.
[Ti] Título:An Unbiased Linkage Approach Reveals That the p53 Pathway Is Coupled to NK Cell Maturation.
[So] Source:J Immunol;199(4):1490-1504, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer cells constitute potent innate lymphoid cells that play a major role in both tumor immunosurveillance and viral clearance via their effector functions. A four-stage model of NK cell functional maturation has been established according to the expression of CD11b and CD27, separating mature NK (mNK) cells into distinct populations that exhibit specific phenotypic and functional properties. To identify genetic factors involved in the regulation of NK cell functional maturation, we performed a linkage analysis on F (B6.Rag1 × NOD.Rag1 intercross) mice. We identified six loci on chromosomes 2, 4, 7, 10, 11, and 18 that were linked to one or more mNK cell subsets. Subsequently, we performed an in silico analysis exploiting mNK cell subset microarray data, highlighting various genes and microRNAs as potential regulators of the functional maturation of NK cells. Together, the combination of our unbiased genetic linkage study and the in silico analysis positions genes known to affect NK cell biology along the specific stages of NK cell functional maturation. Moreover, this approach allowed us to uncover a novel candidate gene in the regulation of NK cell maturation, namely Using mice deficient for , we confirm that this tumor suppressor regulates NK cell functional maturation. Additional candidate genes revealed in this study may eventually serve as targets for the modulation of NK cell functional maturation to potentiate both tumor immunosurveillance and viral clearance.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Ligação Genética
Células Matadoras Naturais/fisiologia
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b/imunologia
Diferenciação Celular
Processos de Crescimento Celular
Células Cultivadas
Simulação por Computador
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/imunologia
Células Matadoras Naturais/imunologia
Camundongos
Camundongos Endogâmicos NOD
MicroRNAs/genética
MicroRNAs/imunologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Homeodomain Proteins); 0 (MicroRNAs); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (Tumor Suppressor Protein p53); 128559-51-3 (RAG-1 protein)
[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:170716
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600789


  9 / 3420 MEDLINE  
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[PMID]:28708898
[Au] Autor:Riau AK; Liu YC; Lim CHL; Lwin NC; Teo EP; Yam GH; Tan DT; Mehta JS
[Ad] Endereço:Tissue Engineering and Stem Cell Group, Singapore Eye Research Institute, Singapore.
[Ti] Título:Retreatment strategies following Small Incision Lenticule Extraction (SMILE): In vivo tissue responses.
[So] Source:PLoS One;12(7):e0180941, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:With any refractive correction, including Small Incision Lenticule Extraction (SMILE), there may be a residual refractive error that requires a retreatment. Here, we investigated the tissue responses following various retreatment procedures in a rabbit model of SMILE. All rabbits underwent a -6.00D correction with SMILE. Two weeks later, they underwent -1.00D enhancement by: (i) VisuMax Circle, followed by excimer ablation (S+C); (ii) secondary SMILE anterior to the primary procedure (S+SE); or (iii) surface ablation (S+P), and were examined for 28 days. S+P induced corneal edema and haze, and more CD11b- (23±6 cells) and TUNEL-positive (36±4 cells) cells in the central stromal superficial layers early post-operatively (p<0.001 compared to other procedures). The corneas appeared normal on day 28 after S+P, but had a lower number of keratocytes near the laser ablated plane compared to other procedures. S+SE and S+C did not induce corneal haze and resulted similar level of fibronectin. However, S+C resulted in more inflammatory (10±2 cells; p = 0.001) and apoptotic cells (25±2 cells; p<0.001) compared to S+SE (7±1 inflammatory cells and 21±3 apoptotic cells) early post-operatively. In conclusion, each SMILE retreatment method resulted in unique tissue responses. S+SE offers advantages, such as minimal inflammation and cell death, as well as maintaining a 'flap-less' surgery, over other procedures. However, depending on the degree of enhancement, the lenticule may become too thin to be extracted and the procedure becomes more difficult to perform than S+C and S+P. S+P can maintain corneal integrity by avoiding flap creation and is technically more simple to perform than the others, but the surgery needs to be supplemented with mitomycin-C in order to reduce inflammation and modulate better wound healing.
[Mh] Termos MeSH primário: Córnea/patologia
Substância Própria/cirurgia
Lasers de Excimer
Ceratectomia Fotorrefrativa
[Mh] Termos MeSH secundário: Animais
Apoptose
Antígeno CD11b/metabolismo
Córnea/diagnóstico por imagem
Córnea/metabolismo
Fibronectinas/metabolismo
Antígeno Ki-67/metabolismo
Microscopia Confocal
Coelhos
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Fibronectins); 0 (Ki-67 Antigen)
[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:170715
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180941


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[PMID]:28698257
[Au] Autor:Li Y; Shen XZ; Li L; Zhao TV; Bernstein KE; Johnson AK; Lyden P; Fang J; Shi P
[Ad] Endereço:From the School of Life Science and Technology, Tongji University, Shanghai, China (Y.L., T.V.Z., J.F.); The Second Affiliated Hospital of Zhejiang University (P.S.), Institute of Translational Medicine (P.S.), and Department of Physiology (X.Z.S.), Zhejiang University School of Medicine, Hangzhou,
[Ti] Título:Brain Transforming Growth Factor-ß Resists Hypertension Via Regulating Microglial Activation.
[So] Source:Stroke;48(9):2557-2564, 2017 Sep.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Hypertension is the major risk factor for stroke. Recent work unveiled that hypertension is associated with chronic neuroinflammation; microglia are the major players in neuroinflammation, and the activated microglia elevate sympathetic nerve activity and blood pressure. This study is to understand how brain homeostasis is kept from hypertensive disturbance and microglial activation at the onset of hypertension. METHODS: Hypertension was induced by subcutaneous delivery of angiotensin II, and blood pressure was monitored in conscious animals. Microglial activity was analyzed by flow cytometry and immunohistochemistry. Antibody, pharmacological chemical, and recombinant cytokine were administered to the brain through intracerebroventricular infusion. Microglial depletion was performed by intracerebroventricular delivering diphtheria toxin to CD11b-diphtheria toxin receptor mice. Gene expression profile in sympathetic controlling nucleus was analyzed by customized qRT-PCR array. RESULTS: Transforming growth factor-ß (TGF-ß) is constitutively expressed in the brains of normotensive mice. Removal of TGF-ß or blocking its signaling before hypertension induction accelerated hypertension progression, whereas supplementation of TGF-ß1 substantially suppressed neuroinflammation, kidney norepinephrine level, and blood pressure. By means of microglial depletion and adoptive transfer, we showed that the effects of TGF-ß on hypertension are mediated through microglia. In contrast to the activated microglia in established hypertension, the resting microglia are immunosuppressive and important in maintaining neural homeostasis at the onset of hypertension. Further, we profiled the signature molecules of neuroinflammation and neuroplasticity associated with hypertension and TGF-ß by qRT-PCR array. CONCLUSIONS: Our results identify that TGF-ß-modulated microglia are critical to keeping brain homeostasis responding to hypertensive disturbance.
[Mh] Termos MeSH primário: Pressão Sanguínea/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Hipertensão/imunologia
Microglia/efeitos dos fármacos
Fator de Crescimento Transformador beta1/farmacologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Angiotensina II/toxicidade
Animais
Pressão Sanguínea/imunologia
Encéfalo/imunologia
Encéfalo/metabolismo
Encéfalo/fisiopatologia
Antígeno CD11b
Toxina Diftérica
Citometria de Fluxo
Fator de Crescimento Semelhante a EGF de Ligação à Heparina
Hipertensão/induzido quimicamente
Hipertensão/genética
Hipertensão/fisiopatologia
Imuno-Histoquímica
Rim/efeitos dos fármacos
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microglia/imunologia
Norepinefrina/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais
Sistema Nervoso Simpático
Transcriptoma
Fator de Crescimento Transformador beta1/imunologia
Vasoconstritores/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Diphtheria Toxin); 0 (Heparin-binding EGF-like Growth Factor); 0 (Transforming Growth Factor beta1); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); X4W3ENH1CV (Norepinephrine)
[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:170713
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017370



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