Base de dados : MEDLINE
Pesquisa : D12.776.543.750.695.160.500.150 [Categoria DeCS]
Referências encontradas : 917 [refinar]
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[PMID]:29274778
[Au] Autor:Stout MC; Narayan S; Pillet ES; Salvino JM; Campbell PM
[Ad] Endereço:Department of Pharmacology & Physiology, College of Medicine, Drexel University, 245 North 15th Street, MS 488, Philadelphia, PA 19102, USA. Electronic address: Matthew.Stout@DrexelMed.edu.
[Ti] Título:Inhibition of CX CR1 reduces cell motility and viability in pancreatic adenocarcinoma epithelial cells.
[So] Source:Biochem Biophys Res Commun;495(3):2264-2269, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased expression of the chemokine CX CL1 and its sole receptor, CX CR1 have been correlated with poor pancreatic cancer patient survival and time to recurrence, as well as with pancreatic perineural invasion. We have previously shown that metastasis of prostate and breast cancer is in part driven by CX CL1, and have developed small molecule inhibitors against the CX CR1 receptor that diminish metastatic burden. Here we ask if inhibition of this chemokine receptor affects the phenotype of PDAC tumor cells. Our findings demonstrate that motility, invasion, and contact-independent growth of PDAC cells all increase following CX CL1 exposure, and that antagonism of CX CR1 by the inhibitor JMS-17-2 reduces each of these phenotypes and correlates with a downregulation of AKT phosphorylation. These data suggest that PDAC tumor cell migration and growth, elements critical in metastatic progression, may susceptible to pharmacologic intervention.
[Mh] Termos MeSH primário: Receptor 1 de Quimiocina CX3C/metabolismo
Carcinoma Ductal Pancreático/metabolismo
Carcinoma Ductal Pancreático/patologia
Movimento Celular
Sobrevivência Celular
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/metabolismo
Linhagem Celular Tumoral
Seres Humanos
Invasividade Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CX3C Chemokine Receptor 1); 0 (CX3CR1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


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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


  3 / 917 MEDLINE  
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[PMID]:28462835
[Au] Autor:Gao M; Wang M; Meyer JA; Peters JS; Zarrinmayeh H; Territo PR; Hutchins GD; Zheng QH
[Ad] Endereço:Department of Radiology and Imaging Sciences, Indiana University School of Medicine, 1345 West 16th Street, Room 202, Indianapolis, IN 46202, USA.
[Ti] Título:Synthesis and preliminary biological evaluation of [ C]methyl (2-amino-5-(benzylthio)thiazolo[4,5-d]pyrimidin-7-yl)-d-leucinate for the fractalkine receptor (CX CR1).
[So] Source:Bioorg Med Chem Lett;27(12):2727-2730, 2017 06 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The reference standard methyl (2-amino-5-(benzylthio)thiazolo[4,5-d]pyrimidin-7-yl)-d-leucinate (5) and its precursor 2-amino-5-(benzylthio)thiazolo[4,5-d]pyrimidin-7-yl)-d-leucine (6) were synthesized from 6-amino-2-mercaptopyrimidin-4-ol and BnBr with overall chemical yield 7% in five steps and 4% in six steps, respectively. The target tracer [ C]methyl (2-amino-5-(benzylthio)thiazolo[4,5-d]pyrimidin-7-yl)-d-leucinate ([ C]5) was prepared from the acid precursor with [ C]CH OTf through O-[ C]methylation and isolated by HPLC combined with SPE in 40-50% radiochemical yield, based on [ C]CO and decay corrected to end of bombardment (EOB). The radiochemical purity was >99%, and the specific activity (SA) at EOB was 370-1110GBq/µmol with a total synthesis time of ∼40-min from EOB. The radioligand depletion experiment of [ C]5 did not display specific binding to CX CR1, and the competitive binding assay of ligand 5 found much lower CX CR1 binding affinity.
[Mh] Termos MeSH primário: Leucina/análogos & derivados
Pirimidinas/farmacologia
Receptores de Quimiocinas/antagonistas & inibidores
Tiazóis/farmacologia
[Mh] Termos MeSH secundário: Receptor 1 de Quimiocina CX3C
Isótopos de Carbono
Relação Dose-Resposta a Droga
Seres Humanos
Leucina/síntese química
Leucina/química
Leucina/farmacologia
Ligantes
Estrutura Molecular
Pirimidinas/síntese química
Pirimidinas/química
Receptores de Quimiocinas/metabolismo
Relação Estrutura-Atividade
Tiazóis/síntese química
Tiazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (CX3CR1 protein, human); 0 (Carbon Isotopes); 0 (Ligands); 0 (Pyrimidines); 0 (Receptors, Chemokine); 0 (Thiazoles); GMW67QNF9C (Leucine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28986258
[Au] Autor:Huang L; Ma B; Ma J; Wang F
[Ad] Endereço:Department of Gastroenterology, General Hospital of NingXia Medical University, Yinchuan, NingXia, 750004, China. Electronic address: txmbw@126.com.
[Ti] Título:Fractalkine/CX3CR1 axis modulated the development of pancreatic ductal adenocarcinoma via JAK/STAT signaling pathway.
[So] Source:Biochem Biophys Res Commun;493(4):1510-1517, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic ductal adenocarcinoma (PDAC) is a fatal malignancy with an estimated 5 year survival rate of approximately 5% of all stages combined. High potential of PDAC metastasis is a leading cause for high mortality and poor prognosis. The majority of patients present with distant metastasis at diagnosis. Fractalkine (FKN) is recognized as a chemokine and a specific ligand of CX3CR1. It has been reported that FKN/CX3CR1 system was upregulated in many types of solid tumors. However, role of FKN/CX3CR1 in PDAC development remains unclear. In the current investigation, we found that FKN and CX3CR1 expression was significantly increased in PDAC tissues, especially in the metastatic samples, and was highly-correlated with severity of PDAC. Ectopic expression of FKN promoted the proliferation and migration of PDAC, while knockdown of CX3CR1 reversed the function of FKN. In addition, PDAC cells with FKN-deficiency showed impaired proliferation and migration activity. The underlying mechanism is that FKN/CX3CR1 activated JAK/STAT signaling, which in turn regulated cell growth. Consistently, in vivo tumorigenesis assay validated the regulatory role of FKN/CX3CR1 in PDAC growth. Our investigation helped understanding the pathogenesis of PDAC occurrence, and demonstrated critical role of FKN/CX3CR1 in PDAC development.
[Mh] Termos MeSH primário: Carcinoma Ductal Pancreático/metabolismo
Quimiocina CX3CL1/metabolismo
Neoplasias Pancreáticas/metabolismo
Receptores de Quimiocinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Receptor 1 de Quimiocina CX3C
Carcinoma Ductal Pancreático/genética
Carcinoma Ductal Pancreático/secundário
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Quimiocina CX3CL1/antagonistas & inibidores
Quimiocina CX3CL1/genética
Técnicas de Silenciamento de Genes
Seres Humanos
Janus Quinases/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias Pancreáticas/etiologia
Neoplasias Pancreáticas/genética
Interferência de RNA
Receptores de Quimiocinas/antagonistas & inibidores
Receptores de Quimiocinas/genética
Fatores de Transcrição STAT/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (CX3CL1 protein, human); 0 (CX3CR1 protein, human); 0 (Chemokine CX3CL1); 0 (Receptors, Chemokine); 0 (STAT Transcription Factors); EC 2.7.10.2 (Janus Kinases)
[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:171008
[St] Status:MEDLINE


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[PMID]:28951447
[Au] Autor:Schecter RW; Maher EE; Welsh CA; Stevens B; Erisir A; Bear MF
[Ad] Endereço:Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139.
[Ti] Título:Experience-Dependent Synaptic Plasticity in V1 Occurs without Microglial CX3CR1.
[So] Source:J Neurosci;37(44):10541-10553, 2017 Nov 01.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brief monocular deprivation (MD) shifts ocular dominance and reduces the density of thalamic synapses in layer 4 of the mouse primary visual cortex (V1). We found that microglial lysosome content is also increased as a result of MD. Previous studies have shown that the microglial fractalkine receptor CX3CR1 is involved in synaptic development and hippocampal plasticity. We therefore tested the hypothesis that neuron-to-microglial communication via CX3CR1 is an essential component of visual cortical development and plasticity in male mice. Our data show that CX3CR1 is not required for normal development of V1 responses to visual stimulation, multiple forms of experience-dependent plasticity, or the synapse loss that accompanies MD in layer 4. By ruling out an essential role for fractalkine signaling, our study narrows the search for understanding how microglia respond to active synapse modification in the visual cortex. Microglia in the visual cortex respond to monocular deprivation with increased lysosome content, but signaling through the fractalkine receptor CX3CR1 is not an essential component in the mechanisms of visual cortical development or experience-dependent synaptic plasticity.
[Mh] Termos MeSH primário: Potenciais Evocados Visuais/fisiologia
Microglia/metabolismo
Plasticidade Neuronal/fisiologia
Receptores de Quimiocinas/deficiência
Córtex Visual/crescimento & desenvolvimento
Córtex Visual/metabolismo
[Mh] Termos MeSH secundário: Animais
Receptor 1 de Quimiocina CX3C
Comunicação Celular/fisiologia
Corpos Geniculados/crescimento & desenvolvimento
Corpos Geniculados/metabolismo
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Técnicas de Cultura de Órgãos
Visão Monocular/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Receptors, Chemokine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2679-16.2017


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[PMID]:28842393
[Au] Autor:Wakita H; Yanagawa T; Kuboi Y; Imai T
[Ad] Endereço:Eisai Co., Ltd., Tsukuba Research Laboratories, Ibaraki (H.W., T.Y., Y.K.) and KAN Research Institute Inc., Hyogo (T.I.), Japan h2-wakita@hhc.eisai.co.jp.
[Ti] Título:E6130, a Novel CX3C Chemokine Receptor 1 (CX3CR1) Modulator, Attenuates Mucosal Inflammation and Reduces CX3CR1 Leukocyte Trafficking in Mice with Colitis.
[So] Source:Mol Pharmacol;92(5):502-509, 2017 Nov.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chemokine fractalkine (CX3C chemokine ligand 1; CX3CL1) and its receptor CX3CR1 are involved in the pathogenesis of several diseases, including inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, rheumatoid arthritis, hepatitis, myositis, multiple sclerosis, renal ischemia, and atherosclerosis. There are no orally available agents that modulate the fractalkine/CX3CR1 axis. [(3 ,4 )-1-[2-Chloro-6-(trifluoromethyl)benzyl]-3-{[1-(cyclohex-1-en-1-ylmethyl)piperidin-4-yl]carbamoyl}-4-methylpyrrolidin-3-yl]acetic acid (2S)-hydroxy(phenyl)acetate (E6130) is an orally available highly selective modulator of CX3CR1 that may be effective for treatment of inflammatory bowel disease. We found that E6130 inhibited the fractalkine-induced chemotaxis of human peripheral blood natural killer cells (IC 4.9 nM), most likely via E6130-induced down-regulation of CX3CR1 on the cell surface. E6130 had agonistic activity via CX3CR1 with respect to guanosine 5'-3- -(thio)triphosphate binding in CX3CR1-expressing Chinese hamster ovary K1 (CHO-K1) membrane and had no antagonistic activity. Orally administered E6130 ameliorated several inflammatory bowel disease-related parameters in a murine CD4 CD45RB T-cell-transfer colitis model and a murine oxazolone-induced colitis model. In the CD4 CD45RB T-cell transfer model, E6130 inhibited the migration of CX3CR1 immune cells and decreased the number of these cells in the gut mucosal membrane. These results suggest that E6130 is a promising therapeutic agent for treatment of inflammatory bowel disease.
[Mh] Termos MeSH primário: Anti-Inflamatórios/administração & dosagem
Quimiotaxia/fisiologia
Colite/metabolismo
Mucosa Intestinal/metabolismo
Leucócitos Mononucleares/metabolismo
Receptores de Quimiocinas/metabolismo
[Mh] Termos MeSH secundário: Administração Oral
Animais
Anti-Inflamatórios/química
Anti-Inflamatórios/metabolismo
Células CHO
Receptor 1 de Quimiocina CX3C
Quimiotaxia/efeitos dos fármacos
Colite/tratamento farmacológico
Colite/patologia
Cricetinae
Cricetulus
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Inflamação/patologia
Mucosa Intestinal/efeitos dos fármacos
Mucosa Intestinal/patologia
Leucócitos Mononucleares/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos SCID
Receptores de Quimiocinas/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Receptors, Chemokine)
[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:170827
[St] Status:MEDLINE
[do] DOI:10.1124/mol.117.108381


  7 / 917 MEDLINE  
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[PMID]:28801233
[Au] Autor:Baratin M; Simon L; Jorquera A; Ghigo C; Dembele D; Nowak J; Gentek R; Wienert S; Klauschen F; Malissen B; Dalod M; Bajénoff M
[Ad] Endereço:Aix Marseille Univ, CNRS, INSERM, CIML, Marseille, France. Electronic address: baratin@ciml.univ-mrs.fr.
[Ti] Título:T Cell Zone Resident Macrophages Silently Dispose of Apoptotic Cells in the Lymph Node.
[So] Source:Immunity;47(2):349-362.e5, 2017 Aug 15.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In lymph nodes (LNs), dendritic cells (DCs) are thought to dispose of apoptotic cells, a function pertaining to macrophages in other tissues. We found that a population of CX3CR1 MERTK cells located in the T cell zone of LNs, previously identified as DCs, are efferocytic macrophages. Lineage-tracing experiments and shield chimeras indicated that these T zone macrophages (TZM) are long-lived macrophages seeded in utero and slowly replaced by blood monocytes after birth. Imaging the LNs of mice in which TZM and DCs express different fluorescent proteins revealed that TZM-and not DCs-act as the only professional scavengers, clearing apoptotic cells in the LN T cell zone in a CX3CR1-dependent manner. Furthermore, similar to other macrophages, TZM appear inefficient in priming CD4 T cells. Thus, efferocytosis and T cell activation in the LN are uncoupled processes designated to macrophages and DCs, respectively, with implications to the maintenance of immune homeostasis.
[Mh] Termos MeSH primário: Linfonodos/imunologia
Macrófagos/imunologia
Fagocitose
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno
Apoptose
Linfócitos T CD4-Positivos/imunologia
Receptor 1 de Quimiocina CX3C
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Células Dendríticas/imunologia
Tolerância Imunológica
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Proto-Oncogênicas/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
Receptores de Quimiocinas/metabolismo
c-Mer Tirosina Quinase
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Proto-Oncogene Proteins); 0 (Receptors, Chemokine); EC 2.7.10.1 (Mertk protein, mouse); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (c-Mer Tyrosine Kinase)
[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:170813
[St] Status:MEDLINE


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[PMID]:28800592
[Au] Autor:Müller I; Pappritz K; Savvatis K; Puhl K; Dong F; El-Shafeey M; Hamdani N; Hamann I; Noutsias M; Infante-Duarte C; Linke WA; Van Linthout S; Tschöpe C
[Ad] Endereço:Charité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
[Ti] Título:CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
[So] Source:PLoS One;12(8):e0182643, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro-inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis.
[Mh] Termos MeSH primário: Quimiocina CX3CL1/imunologia
Infecções por Coxsackievirus/genética
Enterovirus Humano B/patogenicidade
Interações Hospedeiro-Patógeno/imunologia
Miocardite/genética
Receptores de Quimiocinas/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Receptor 1 de Quimiocina CX3C
Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/imunologia
Quimiocina CX3CL1/genética
Infecções por Coxsackievirus/imunologia
Infecções por Coxsackievirus/patologia
Infecções por Coxsackievirus/virologia
Modelos Animais de Doenças
Enterovirus Humano B/crescimento & desenvolvimento
Regulação da Expressão Gênica
Testes de Função Cardíaca
Seres Humanos
Interleucinas/genética
Interleucinas/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocardite/imunologia
Miocardite/patologia
Miocardite/virologia
Miócitos Cardíacos/imunologia
Miócitos Cardíacos/patologia
Fosforilação
Proteínas Quinases/genética
Proteínas Quinases/imunologia
Receptores de Quimiocinas/deficiência
Receptores de Quimiocinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cell Adhesion Molecules); 0 (Chemokine CX3CL1); 0 (Cx3cl1 protein, mouse); 0 (Cx3cr1 protein, mouse); 0 (Interleukins); 0 (Receptors, Chemokine); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (titin protein, mouse)
[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:170812
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182643


  9 / 917 MEDLINE  
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[PMID]:28723545
[Au] Autor:Muller PA; Mucida D
[Ad] Endereço:Laboratory of Mucosal Immunology, The Rockefeller University, 1230 York Ave, New York, NY 10065, USA. Electronic address: pmuller@rockefeller.edu.
[Ti] Título:Spineless Behavior of CX3CR1 Monocytes in Response to Infection.
[So] Source:Immunity;47(1):12-14, 2017 Jul 18.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sickness in mammals can lead to cognition deficits, although the underlying mechanisms remain elusive. In a recent Nature Medicine article, Garré et al. (2017) report that sickness-induced cortical dendritic spine loss and impaired memory formation is mediated by CX3CR1 monocyte-derived TNF-α.
[Mh] Termos MeSH primário: Espinhas Dendríticas/fisiologia
Transtornos Mentais/imunologia
Monócitos/fisiologia
Neurônios Motores/fisiologia
Rede Nervosa
Plasticidade Neuronal
Viroses/imunologia
[Mh] Termos MeSH secundário: Animais
Receptor 1 de Quimiocina CX3C
Seres Humanos
Memória
Transtornos Mentais/etiologia
Transtornos Mentais/psicologia
Camundongos
Monócitos/virologia
Neurônios Motores/virologia
Poli I-C/imunologia
Receptores de Quimiocinas/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Viroses/complicações
Viroses/psicologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Receptors, Chemokine); 0 (Tumor Necrosis Factor-alpha); O84C90HH2L (Poly I-C)
[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:170721
[St] Status:MEDLINE


  10 / 917 MEDLINE  
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[PMID]:28722110
[Au] Autor:Liao X; Ren J; Reihl A; Pirapakaran T; Sreekumar B; Cecere TE; Reilly CM; Luo XM
[Ad] Endereço:Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
[Ti] Título:Renal-infiltrating CD11c cells are pathogenic in murine lupus nephritis through promoting CD4 T cell responses.
[So] Source:Clin Exp Immunol;190(2):187-200, 2017 Nov.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lupus nephritis (LN) is a major manifestation of systemic lupus erythematosus (SLE), causing morbidity and mortality in 40-60% of SLE patients. The pathogenic mechanisms of LN are not completely understood. Recent studies have demonstrated the presence of various immune cell populations in lupus nephritic kidneys of both SLE patients and lupus-prone mice. These cells may play important pathogenic or regulatory roles in situ to promote or sustain LN. Here, using lupus-prone mouse models, we showed the pathogenic role of a kidney-infiltrating CD11c myeloid cell population in LN. These CD11c cells accumulated in the kidneys of lupus-prone mice as LN progressed. Surface markers of this population suggest their dendritic cell identity and differentiation from lymphocyte antigen 6 complex (Ly6C) mature monocytes. The cytokine/chemokine profile of these renal-infiltrating CD11c cells suggests their roles in promoting LN, which was confirmed further in a loss-of-function in-vivo study by using an antibody-drug conjugate (ADC) strategy targeting CX CR1, a chemokine receptor expressed highly on these CD11c cells. However, CX CR1 was dispensable for the homing of CD11c cells into lupus nephritic kidneys. Finally, we found that these CD11c cells co-localized with infiltrating T cells in the kidney. Using an ex- vivo co-culture system, we showed that renal-infiltrating CD11c cells promoted the survival, proliferation and interferon-γ production of renal-infiltrating CD4 T cells, suggesting a T cell-dependent mechanism by which these CD11c cells promote LN. Together, our results identify a pathogenic kidney-infiltrating CD11c cell population promoting LN progression, which could be a new therapeutic target for the treatment of LN.
[Mh] Termos MeSH primário: Antígeno CD11c/imunologia
Linfócitos T CD4-Positivos/imunologia
Rim/imunologia
Nefrite Lúpica/imunologia
Células Mieloides/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/imunologia
Receptor 1 de Quimiocina CX3C
Movimento Celular
Quimiocinas/imunologia
Técnicas de Cocultura
Citocinas/imunologia
Células Dendríticas/imunologia
Modelos Animais de Doenças
Interferon gama/biossíntese
Interferon gama/imunologia
Rim/patologia
Nefrite Lúpica/fisiopatologia
Camundongos
Células Mieloides/imunologia
Receptores de Quimiocinas/genética
Receptores de Quimiocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (CD11c Antigen); 0 (CX3C Chemokine Receptor 1); 0 (Chemokines); 0 (Cx3cr1 protein, mouse); 0 (Cytokines); 0 (Ly6 protein, mouse); 0 (Receptors, Chemokine); 82115-62-6 (Interferon-gamma)
[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:170720
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13017



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