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[PMID]:28462530
[Au] Autor:Blander JM
[Ad] Endereço:Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY, USA.
[Ti] Título:The many ways tissue phagocytes respond to dying cells.
[So] Source:Immunol Rev;277(1):158-173, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Apoptosis is an important component of normal tissue physiology, and the prompt removal of apoptotic cells is equally essential to avoid the undesirable consequences of their accumulation and disintegration. Professional phagocytes are highly specialized for engulfing apoptotic cells. The recent ability to track cells that have undergone apoptosis in situ has revealed a division of labor among the tissue resident phagocytes that sample them. Macrophages are uniquely programmed to process internalized apoptotic cell-derived fatty acids, cholesterol and nucleotides, as a reflection of their dominant role in clearing the bulk of apoptotic cells. Dendritic cells carry apoptotic cells to lymph nodes where they signal the emergence and expansion of highly suppressive regulatory CD4 T cells. A broad suppression of inflammation is executed through distinct phagocyte-specific mechanisms. A clever induction of negative regulatory nodes is notable in dendritic cells serving to simultaneously shut down multiple pathways of inflammation. Several of the genes and pathways modulated in phagocytes in response to apoptotic cells have been linked to chronic inflammatory and autoimmune diseases such as atherosclerosis, inflammatory bowel disease and systemic lupus erythematosus. Our collective understanding of old and new phagocyte functions after apoptotic cell phagocytosis demonstrates the enormity of ways to mediate immune suppression and enforce tissue homeostasis.
[Mh] Termos MeSH primário: Aterosclerose/imunologia
Doenças Inflamatórias Intestinais/imunologia
Fagócitos/fisiologia
Fagocitose
[Mh] Termos MeSH secundário: Animais
Apoptose
Colesterol/metabolismo
Células Dendríticas/imunologia
Ácidos Graxos/metabolismo
Homeostase
Seres Humanos
Tolerância Imunológica
Lúpus Eritematoso Sistêmico
Nucleotídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Nucleotides); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12537


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[PMID]:29326275
[Au] Autor:Leonardi I; Li X; Semon A; Li D; Doron I; Putzel G; Bar A; Prieto D; Rescigno M; McGovern DPB; Pla J; Iliev ID
[Ad] Endereço:Gastroenterology and Hepatology Division, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, New York, NY 10021, USA.
[Ti] Título:CX3CR1 mononuclear phagocytes control immunity to intestinal fungi.
[So] Source:Science;359(6372):232-236, 2018 01 12.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intestinal fungi are an important component of the microbiota, and recent studies have unveiled their potential in modulating host immune homeostasis and inflammatory disease. Nonetheless, the mechanisms governing immunity to gut fungal communities (mycobiota) remain unknown. We identified CX3CR1 mononuclear phagocytes (MNPs) as being essential for the initiation of innate and adaptive immune responses to intestinal fungi. CX3CR1 MNPs express antifungal receptors and activate antifungal responses in a Syk-dependent manner. Genetic ablation of CX3CR1 MNPs in mice led to changes in gut fungal communities and to severe colitis that was rescued by antifungal treatment. In Crohn's disease patients, a missense mutation in the gene encoding CX3CR1 was identified and found to be associated with impaired antifungal responses. These results unravel a role of CX3CR1 MNPs in mediating interactions between intestinal mycobiota and host immunity at steady state and during inflammatory disease.
[Mh] Termos MeSH primário: Receptor 1 de Quimiocina CX3C/análise
Receptor 1 de Quimiocina CX3C/genética
Candida albicans/imunologia
Microbioma Gastrointestinal/imunologia
Intestinos/microbiologia
Micobioma/imunologia
Fagócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antifúngicos/biossíntese
Anticorpos Antifúngicos/sangue
Candida albicans/crescimento & desenvolvimento
Colite/tratamento farmacológico
Colite/microbiologia
Doença de Crohn/genética
Doença de Crohn/imunologia
Células Dendríticas/imunologia
Microbioma Gastrointestinal/fisiologia
Seres Humanos
Imunidade nas Mucosas
Imunoglobulina G/biossíntese
Imunoglobulina G/sangue
Intestinos/imunologia
Camundongos
Mutação de Sentido Incorreto
Micobioma/fisiologia
Fagócitos/microbiologia
Linfócitos T Reguladores/imunologia
Células Th17/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Fungal); 0 (CX3C Chemokine Receptor 1); 0 (CX3CR1 protein, human); 0 (Cx3cr1 protein, mouse); 0 (Immunoglobulin G)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1126/science.aao1503


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[PMID]:27776109
[Au] Autor:Buttgereit A; Lelios I; Yu X; Vrohlings M; Krakoski NR; Gautier EL; Nishinakamura R; Becher B; Greter M
[Ad] Endereço:Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
[Ti] Título:Sall1 is a transcriptional regulator defining microglia identity and function.
[So] Source:Nat Immunol;17(12):1397-1406, 2016 Dec.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microglia are the resident macrophages of the central nervous system (CNS). Gene expression profiling has identified Sall1, which encodes a transcriptional regulator, as a microglial signature gene. We found that Sall1 was expressed by microglia but not by other members of the mononuclear phagocyte system or by other CNS-resident cells. Using Sall1 for microglia-specific gene targeting, we found that the cytokine receptor CSF1R was involved in the maintenance of adult microglia and that the receptor for the cytokine TGF-ß suppressed activation of microglia. We then used the microglia-specific expression of Sall1 to inducibly inactivate the murine Sall1 locus in vivo, which resulted in the conversion of microglia from resting tissue macrophages into inflammatory phagocytes, leading to altered neurogenesis and disturbed tissue homeostasis. Collectively, our results show that transcriptional regulation by Sall1 maintains microglial identity and physiological properties in the CNS and allows microglia-specific manipulation in vivo.
[Mh] Termos MeSH primário: Microglia/fisiologia
Fagócitos/imunologia
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/metabolismo
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Perfilação da Expressão Gênica
Inativação Gênica
Homeostase/genética
Mediadores da Inflamação/metabolismo
Ativação de Macrófagos/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurogênese/genética
Fatores de Transcrição/genética
Transcriptoma
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Csf1r protein, mouse); 0 (Inflammation Mediators); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 0 (Receptors, Transforming Growth Factor beta); 0 (Sall1 protein, mouse); 0 (Transcription Factors); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3585


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[PMID]:29183754
[Au] Autor:Santos GB; Ribeiro ACG; Lima SNP; Trostchansky A; Cerdeira CD; Brigagão MRPL
[Ad] Endereço:Departamento de Bioquímica, Instituto de Ciências Biomédicas, Universidade Federal de Alfenas, Alfenas, MG, Brazil.
[Ti] Título:Nitroxide Tempol down-regulates kinase activities associated with NADPH oxidase function in phagocytic cells and potentially decreases their fungicidal response.
[So] Source:Chem Biol Interact;279:203-209, 2018 Jan 05.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:AIMS: The identification of novel targets to control inflammation in humans is probably the primary challenge that impairs the development of new anti-inflammatory drugs. Therefore, the modulation of intracellular signaling pathways in phagocytes may be an interesting means of achieving this goal. However, this change to signaling can compromise the host's susceptibility to invading pathogens. We investigated whether the antioxidant nitroxide Tempol regulates the activity of kinases associated with the production of oxidants in neutrophils, which affects the fungicidal capability of these cells. MAIN METHODS: The effects of Tempol on PMA- or fMLP-activated neutrophils were examined by oxygen consumption as an index of the oxidative burst, a release of extracellular and total Reactive Oxygen Species (ROS) by chemiluminescence, kinase activities through analysis of ATP consumption during enzyme activities and the dot blot immunoassay and, finally, by neutrophil capacity of killing Candida albicans. KEY FINDINGS: Tempol significantly inhibited the neutrophil oxidative burst in a concentration-dependent manner and decreased oxygen consumption (IC50 = 45 µM) and extracellular/total ROS formation with an increase on the lag period response. In addition, Tempol inhibited neutrophil kinase activities (i.e., a decrease in protein phosphorylation) elicited through different biochemical pathways and consequently impaired the fungicidal activity of these cells. SIGNIFICANCE: Although Tempol has potential anti-inflammatory activity that acts on different intracellular pathways (such as those involving kinases), researchers should be cautious, since this nitroxide down-regulated oxidants production and the fungicidal response of neutrophils.
[Mh] Termos MeSH primário: Candida albicans/fisiologia
Óxidos N-Cíclicos/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
NADPH Oxidases/metabolismo
Fagócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Óxidos N-Cíclicos/química
Regulação para Baixo/efeitos dos fármacos
Inflamação
Masculino
Camundongos
Estrutura Molecular
Neutrófilos/enzimologia
Consumo de Oxigênio
Fosfotransferases/genética
Fosfotransferases/metabolismo
Marcadores de Spin
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic N-Oxides); 0 (Spin Labels); EC 1.6.3.- (NADPH Oxidases); EC 2.7.- (Phosphotransferases); U78ZX2F65X (tempol)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


  5 / 7387 MEDLINE  
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[PMID]:29240825
[Au] Autor:Santiago-Tirado FH; Doering TL
[Ad] Endereço:Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
[Ti] Título:False friends: Phagocytes as Trojan horses in microbial brain infections.
[So] Source:PLoS Pathog;13(12):e1006680, 2017 12.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Meningite/imunologia
Meningite/microbiologia
Fagócitos/imunologia
Fagócitos/microbiologia
[Mh] Termos MeSH secundário: Encéfalo/imunologia
Encéfalo/microbiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006680


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[PMID]:29045901
[Au] Autor:Zanoni I; Tan Y; Di Gioia M; Springstead JR; Kagan JC
[Ad] Endereço:Harvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, MA, USA; Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy. Electronic address: ivan.zanoni@childrens.harvard.edu.
[Ti] Título:By Capturing Inflammatory Lipids Released from Dying Cells, the Receptor CD14 Induces Inflammasome-Dependent Phagocyte Hyperactivation.
[So] Source:Immunity;47(4):697-709.e3, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A heterogeneous mixture of lipids called oxPAPC, derived from dying cells, can hyperactivate dendritic cells (DCs) but not macrophages. Hyperactive DCs are defined by their ability to release interleukin-1 (IL-1) while maintaining cell viability, endowing these cells with potent aptitude to stimulate adaptive immunity. Herein, we found that the bacterial lipopolysaccharide receptor CD14 captured extracellular oxPAPC and delivered these lipids into the cell to promote inflammasome-dependent DC hyperactivation. Notably, we identified two specific components within the oxPAPC mixture that hyperactivated macrophages, allowing these cells to release IL-1 for several days, by a CD14-dependent process. In murine models of sepsis, conditions that promoted cell hyperactivation resulted in inflammation but not lethality. Thus, multiple phagocytes are capable of hyperactivation in response to oxPAPC, with CD14 acting as the earliest regulator in this process, serving to capture and transport these lipids to promote inflammatory cell fate decisions.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Inflamassomos/imunologia
Receptores de Lipopolissacarídeos/imunologia
Fagócitos/imunologia
Fosfatidilcolinas/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Animais
Western Blotting
Linhagem Celular
Sobrevivência Celular/imunologia
Células Dendríticas/metabolismo
Endocitose/efeitos dos fármacos
Endocitose/imunologia
Feminino
Citometria de Fluxo
Células HEK293
Seres Humanos
Inflamassomos/metabolismo
Interleucina-1/imunologia
Interleucina-1/metabolismo
Receptores de Lipopolissacarídeos/genética
Receptores de Lipopolissacarídeos/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fagócitos/metabolismo
Fosfatidilcolinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Interleukin-1); 0 (Lipopolysaccharide Receptors); 0 (Lipopolysaccharides); 0 (Phosphatidylcholines); 0 (oxidized-L-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine)
[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:171019
[St] Status:MEDLINE


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[PMID]:29036184
[Au] Autor:Fernández AG; Hielpos MS; Ferrero MC; Fossati CA; Baldi PC
[Ad] Endereço:Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Cátedra de Inmunología, Buenos Aires, Argentina.
[Ti] Título:Proinflammatory response of canine trophoblasts to Brucella canis infection.
[So] Source:PLoS One;12(10):e0186561, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brucella canis infection is an important cause of late-term abortion in pregnant bitches. The pathophysiological mechanisms leading to B. canis-induced abortion are unknown, but heavily infected trophoblasts are consistently observed. As trophoblasts responses to other pathogens contribute to placental inflammation leading to abortion, the aim of the present study was to characterize the cytokine response of canine trophoblasts to B. canis infection. To achieve this, trophoblasts isolated from term placenta of healthy female dogs were infected with B. canis, culture supernatants were harvested for cytokine determinations, and the load of intracellular viable B. canis was determined at different times post-infection. Additionally, cytokine responses were assessed in non-infected trophoblasts stimulated with conditioned media (CM) from B. canis-infected canine monocytes and neutrophils. Finally, cytokine response and bacteria replication were assessed in canine placental explants infected ex vivo. B. canis successfully infected and replicated in primary canine trophoblasts, eliciting an increase in IL-8 and RANTES (CCL5) secretion. Moreover, the stimulation of trophoblasts with CM from B. canis-infected monocytes and neutrophils induced a significant increase in IL-8, IL-6 and RANTES secretion. B. canis replication was confirmed in infected placental explants and the infection elicited an increased secretion of TNF-α, IL-8, IL-6 and RANTES. This study shows that canine trophoblasts produce proinflammatory cytokines in response to B. canis infection and/or to stimulation with factors produced by infected monocytes and neutrophils. These cytokines may contribute to placental inflammation leading to abortion in B. canis-infected pregnant bitches.
[Mh] Termos MeSH primário: Brucella canis/fisiologia
Trofoblastos/microbiologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Bactérias/imunologia
Brucella canis/imunologia
Quimiocinas/metabolismo
Cães
Feminino
Inflamação/microbiologia
Fagócitos/citologia
Placenta/microbiologia
Gravidez
Receptores Toll-Like/agonistas
Trofoblastos/citologia
Trofoblastos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Chemokines); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186561


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[PMID]:28979997
[Au] Autor:Crespo-Garcia S; Corkhill C; Roubeix C; Davids AM; Kociok N; Strauss O; Joussen AM; Reichhart N
[Ti] Título:Inhibition of Placenta Growth Factor Reduces Subretinal Mononuclear Phagocyte Accumulation in Choroidal Neovascularization.
[So] Source:Invest Ophthalmol Vis Sci;58(12):4997-5006, 2017 Oct 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: The cellular immune response driven by mononuclear phagocytes (MPs) is crucial for choroidal neovascularization (CNV) progression. Case reports show that a switch from pure anti-vascular endothelial growth factor-A (VEGF-A) intravitreal treatment to aflibercept, a drug with combined anti-VEGF-A and anti-placenta growth factor (PlGF) activity, can be beneficial for patients who do not respond to anti-VEGF-A alone. Since MPs harbor VEGFR1, we hypothesize that the interplay of P1GF/vascular endothelial growth factor receptor 1 (VEGFR1) in immune cells plays a pivotal role for CNV. Methods: CNV was induced with laser, and immune cells and neovascularization were analyzed in vivo and ex vivo. Immunohistochemistry was employed for protein detection. Differential expression of angiogenic factors and macrophage polarization markers were assessed by quantitative PCR (qPCR). One day after laser, intravitreal injection of aflibercept or anti-PlGF was performed. Results: In the early inflammatory phase after laser, Plgf but not Vegfa was significantly upregulated. VEGF-A upregulation is limited to the scar, whereas PlGF shows a wider distribution. M1 (proinflammatory) macrophage markers were upregulated in the early phase of CNV. However, M2 (proangiogenic) markers showed more inconsistent dynamics. We demonstrated that both aflibercept and anti-PlGF treatments decrease the overall amount of activated subretinal MPs, and especially of those expressing PlGF. These data correlated with a reduction in leakage associated to CNV. Aflibercept showed a stronger reduction in both parameters. Conclusions: The results hint at an interplay between PlGF/VEGFR1 and MPs that is important in the early phase of CNV. A combined inhibition of VEGF-A and PlGF is superior to a specific anti-PlGF treatment in terms of subretinal MP recruitment.
[Mh] Termos MeSH primário: Neovascularização de Coroide/imunologia
Fagócitos/imunologia
Fator de Crescimento Placentário/antagonistas & inibidores
Retina/imunologia
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/farmacologia
Animais
Anticorpos Bloqueadores/farmacologia
Proteínas de Ligação ao Cálcio
Neovascularização de Coroide/tratamento farmacológico
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Regulação da Expressão Gênica
Fatores Imunológicos/farmacologia
Injeções Intravítreas
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas dos Microfilamentos
Microscopia de Fluorescência
Oftalmoscopia
Fator de Crescimento Placentário/genética
Reação em Cadeia da Polimerase em Tempo Real
Receptores de Fatores de Crescimento do Endotélio Vascular
Proteínas Recombinantes de Fusão/farmacologia
Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores
Fator A de Crescimento do Endotélio Vascular/genética
Receptor 1 de Fatores de Crescimento do Endotélio Vascular/genética
Degeneração Macular Exsudativa/tratamento farmacológico
Degeneração Macular Exsudativa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Angiogenesis Inhibitors); 0 (Antibodies, Blocking); 0 (Calcium-Binding Proteins); 0 (Immunologic Factors); 0 (Microfilament Proteins); 0 (Pgf protein, mouse); 0 (Recombinant Fusion Proteins); 0 (Vascular Endothelial Growth Factor A); 0 (vascular endothelial growth factor A, mouse); 144589-93-5 (Placenta Growth Factor); 15C2VL427D (aflibercept); EC 2.7.10.1 (Flt1 protein, mouse); EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.16-21283


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[PMID]:28942921
[Au] Autor:Wang Y; Subramanian M; Yurdagul A; Barbosa-Lorenzi VC; Cai B; de Juan-Sanz J; Ryan TA; Nomura M; Maxfield FR; Tabas I
[Ad] Endereço:Department of Medicine, Columbia University, New York, NY 10032, USA.
[Ti] Título:Mitochondrial Fission Promotes the Continued Clearance of Apoptotic Cells by Macrophages.
[So] Source:Cell;171(2):331-345.e22, 2017 Oct 05.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Clearance of apoptotic cells (ACs) by phagocytes (efferocytosis) prevents post-apoptotic necrosis and dampens inflammation. Defective efferocytosis drives important diseases, including atherosclerosis. For efficient efferocytosis, phagocytes must be able to internalize multiple ACs. We show here that uptake of multiple ACs by macrophages requires dynamin-related protein 1 (Drp1)-mediated mitochondrial fission, which is triggered by AC uptake. When mitochondrial fission is disabled, AC-induced increase in cytosolic calcium is blunted owing to mitochondrial calcium sequestration, and calcium-dependent phagosome formation around secondarily encountered ACs is impaired. These defects can be corrected by silencing the mitochondrial calcium uniporter (MCU). Mice lacking myeloid Drp1 showed defective efferocytosis and its pathologic consequences in the thymus after dexamethasone treatment and in advanced atherosclerotic lesions in fat-fed Ldlr mice. Thus, mitochondrial fission in response to AC uptake is a critical process that enables macrophages to clear multiple ACs and to avoid the pathologic consequences of defective efferocytosis in vivo.
[Mh] Termos MeSH primário: Macrófagos/citologia
Dinâmica Mitocondrial
[Mh] Termos MeSH secundário: Animais
Apoptose
Seres Humanos
Macrófagos/metabolismo
Camundongos
Proteínas Associadas aos Microtúbulos/metabolismo
Mitocôndrias/metabolismo
Células Mieloides/metabolismo
Fagócitos/metabolismo
Fagossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


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[PMID]:28926543
[Au] Autor:Kaplan DH
[Ad] Endereço:Department of Dermatology and Department of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
[Ti] Título:Ontogeny and function of murine epidermal Langerhans cells.
[So] Source:Nat Immunol;18(10):1068-1075, 2017 Sep 19.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Langerhans cells (LCs) are epidermis-resident antigen-presenting cells that share a common ontogeny with macrophages but function as dendritic cells (DCs). Their development, recruitment and retention in the epidermis is orchestrated by interactions with keratinocytes through multiple mechanisms. LC and dermal DC subsets often show functional redundancy, but LCs are required for specific types of adaptive immune responses when antigen is concentrated in the epidermis. This Review will focus on those developmental and functional properties that are unique to LCs.
[Mh] Termos MeSH primário: Epiderme/imunologia
Epiderme/metabolismo
Células de Langerhans/imunologia
Células de Langerhans/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Apresentadoras de Antígenos/imunologia
Células Apresentadoras de Antígenos/metabolismo
Biomarcadores
Comunicação Celular
Diferenciação Celular
Apresentação Cruzada
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Suscetibilidade a Doenças
Queratinócitos/metabolismo
Ativação Linfocitária
Camundongos
Fagócitos/imunologia
Fagócitos/metabolismo
Fenótipo
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3815



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