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Pesquisa : D12.644.276.374.200.110.890 [Categoria DeCS]
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[PMID]:28467903
[Au] Autor:Vaahtomeri K; Brown M; Hauschild R; De Vries I; Leithner AF; Mehling M; Kaufmann WA; Sixt M
[Ad] Endereço:Institute of Science and Technology Austria (IST Austria), Am Campus 1, 3400 Klosterneuburg, Austria; Wihuri Research Institute and Translational Cancer Biology Program, Research Program Unit, University of Helsinki, Biomedicum Helsinki, Haartmaninkatu 8, 00290 Helsinki, Finland. Electronic address:
[Ti] Título:Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.
[So] Source:Cell Rep;19(5):902-909, 2017 May 02.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration.
[Mh] Termos MeSH primário: Quimiocina CCL21/metabolismo
Células Dendríticas/fisiologia
Células Endoteliais/fisiologia
Endotélio Linfático/citologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Quimiocina CCL21/secreção
Células Dendríticas/metabolismo
Células Endoteliais/metabolismo
Endotélio Linfático/fisiologia
Feminino
Junções Intercelulares/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL21)
[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:170504
[St] Status:MEDLINE


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[PMID]:28935759
[Au] Autor:Karlsen TV; Reikvam T; Tofteberg A; Nikpey E; Skogstrand T; Wagner M; Tenstad O; Wiig H
[Ad] Endereço:From the Department of Biomedicine, University of Bergen, Norway (T.V.K., T.R., A.T., E.N., T.S., M.W., O.T., H.W.); and Departments of Medicine (E.N.) and Pathology (M.W.), Haukeland University Hospital, Bergen, Norway. tine.karlsen@uib.no helge.wiig@uib.no.
[Ti] Título:Lymphangiogenesis Facilitates Initial Lymph Formation and Enhances the Dendritic Cell Mobilizing Chemokine CCL21 Without Affecting Migration.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2128-2135, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Lymphatic vessels play an important role in body fluid, as well as immune system homeostasis. Although the role of malfunctioning or missing lymphatics has been studied extensively, less is known on the functional consequences of a chronically expanded lymphatic network or lymphangiogenesis. APPROACH AND RESULTS: To this end, we used K14-VEGF-C (keratin-14 vascular endothelial growth factor-C) transgenic mice overexpressing the vascular endothelial growth factor C in skin and investigated the responses to inflammatory and fluid volume challenges. We also recorded interstitial fluid pressure, a major determinant of lymph flow. Transgenic mice had a strongly enhanced lymph vessel area in skin. Acute inflammation induced by lipopolysaccharide and chronic inflammation by delayed-type hypersensitivity both resulted in increased interstitial fluid pressure and reduced lymph flow, both to the same extent in wild-type and transgenic mice. Hyperplastic lymphatic vessels, however, demonstrated enhanced transport capacity after local fluid overload not induced by inflammation. In this situation, interstitial fluid pressure was increased to a similar extent in the 2 strains, thus, suggesting that the enhanced lymph vessel area facilitated initial lymph formation. The increased lymph vessel area resulted in an enhanced production of the chemoattractant CCL21 that, however, did not result in augmented dendritic cell migration after induction of local skin inflammation by fluorescein isothiocyanate. CONCLUSIONS: An expanded lymphatic network is capable of enhanced chemoattractant production, and lymphangiogenesis will facilitate initial lymph formation favoring increased clearance of fluid in situations of augmented fluid filtration.
[Mh] Termos MeSH primário: Quimiocina CCL21/metabolismo
Quimiotaxia
Células Dendríticas/metabolismo
Dermatite Alérgica de Contato/metabolismo
Linfa/metabolismo
Linfangiogênese
Vasos Linfáticos/metabolismo
Linfedema/metabolismo
[Mh] Termos MeSH secundário: Animais
Dermatite Alérgica de Contato/genética
Dermatite Alérgica de Contato/patologia
Dermatite Alérgica de Contato/fisiopatologia
Modelos Animais de Doenças
Líquido Extracelular/metabolismo
Feminino
Deslocamentos de Líquidos Corporais
Fluoresceína-5-Isotiocianato
Genótipo
Queratina-14/genética
Lipopolissacarídeos
Vasos Linfáticos/patologia
Vasos Linfáticos/fisiopatologia
Linfedema/genética
Linfedema/patologia
Linfedema/fisiopatologia
Masculino
Camundongos Endogâmicos C3H
Camundongos Transgênicos
Oxazolona
Fenótipo
Pressão
Regiões Promotoras Genéticas
Transdução de Sinais
Fatores de Tempo
Regulação para Cima
Fator C de Crescimento do Endotélio Vascular/genética
Fator C de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL21); 0 (Keratin-14); 0 (Lipopolysaccharides); 0 (Vascular Endothelial Growth Factor C); 15646-46-5 (Oxazolone); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309883


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[PMID]:28808159
[Au] Autor:Machelart A; Khadrawi A; Demars A; Willemart K; De Trez C; Letesson JJ; Muraille E
[Ad] Endereço:Unité de Recherche en Biologie des Microorganismes, Laboratoire d'Immunologie et de Microbiologie, Université de Namur, Namur, Belgium.
[Ti] Título:Chronic Brucella Infection Induces Selective and Persistent Interferon Gamma-Dependent Alterations of Marginal Zone Macrophages in the Spleen.
[So] Source:Infect Immun;85(11), 2017 Nov.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The spleen is known as an important filter for blood-borne pathogens that are trapped by specialized macrophages in the marginal zone (MZ): the CD209 MZ macrophages (MZMs) and the CD169 marginal metallophilic macrophages (MMMs). Acute systemic infection strongly impacts MZ populations and the location of T and B lymphocytes. This phenomenon has been linked to reduced chemokine secretion by stromal cells. spp. are the causative agent of brucellosis, a widespread zoonotic disease. Here, we used infection as a model to investigate the impact of chronic stealth infection on splenic MZ macrophage populations. During the late phase of infection, we observed a loss of both MZMs and MMMs, with a durable disappearance of MZMs, leading to a reduction of the ability of the spleen to take up soluble antigens, beads, and unrelated bacteria. This effect appears to be selective as every other lymphoid and myeloid population analyzed increased during infection, which was also observed following and infection. Comparison of wild-type and deficient mice suggested that MZ macrophage population loss is dependent on interferon gamma (IFN-γ) receptor but independent of T cells or tumor necrosis factor alpha receptor 1 (TNF-αR1) signaling pathways and is not correlated to an alteration of CCL19, CCL21, and CXCL13 chemokine mRNA expression. Our results suggest that MZ macrophage populations are particularly sensitive to persistent low-level IFN-γ-mediated inflammation and that infection could reduce the ability of the spleen to perform certain MZM- and MMM-dependent tasks, such as antigen delivery to lymphocytes and control of systemic infection.
[Mh] Termos MeSH primário: Brucelose/imunologia
Interações Hospedeiro-Patógeno
Interferon gama/imunologia
Macrófagos/imunologia
Receptores de Interferon/imunologia
Baço/imunologia
[Mh] Termos MeSH secundário: Animais
Antibacterianos/farmacologia
Linfócitos B/imunologia
Linfócitos B/microbiologia
Brucella abortus/efeitos dos fármacos
Brucella abortus/imunologia
Brucella abortus/patogenicidade
Brucella melitensis/efeitos dos fármacos
Brucella melitensis/imunologia
Brucella melitensis/patogenicidade
Brucella suis/efeitos dos fármacos
Brucella suis/imunologia
Brucella suis/patogenicidade
Brucelose/tratamento farmacológico
Brucelose/genética
Brucelose/microbiologia
Quimiocina CCL19/genética
Quimiocina CCL19/imunologia
Quimiocina CCL21/genética
Quimiocina CCL21/imunologia
Quimiocina CXCL13/genética
Quimiocina CXCL13/imunologia
Doença Crônica
Regulação da Expressão Gênica
Interferon gama/genética
Macrófagos/microbiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
RNA Mensageiro/genética
RNA Mensageiro/imunologia
Receptores de Interferon/deficiência
Receptores de Interferon/genética
Receptores Tipo I de Fatores de Necrose Tumoral/deficiência
Receptores Tipo I de Fatores de Necrose Tumoral/genética
Receptores Tipo I de Fatores de Necrose Tumoral/imunologia
Rifampina/farmacologia
Transdução de Sinais
Baço/microbiologia
Estreptomicina/farmacologia
Linfócitos T/imunologia
Linfócitos T/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Ccl19 protein, mouse); 0 (Chemokine CCL19); 0 (Chemokine CCL21); 0 (Chemokine CXCL13); 0 (Cxcl13 protein, mouse); 0 (RNA, Messenger); 0 (Receptors, Interferon); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (interferon gamma receptor); 82115-62-6 (Interferon-gamma); VJT6J7R4TR (Rifampin); Y45QSO73OB (Streptomycin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28796037
[Au] Autor:Ruan L; Yang Y; Huang Y; Ding L; Zhang C; Wu X
[Ad] Endereço:Department of Gerontology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
[Ti] Título:Functional prediction of miR-3144-5p in human cardiac myocytes based on transcriptome sequencing and bioinformatics.
[So] Source:Medicine (Baltimore);96(32):e7539, 2017 Aug.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: RAN guanine nucleotide release factor (RANGRF) encoding protein MOG1 plays an important role in cardiac arrhythmia, so we intended to investigate the regulatory miRNA of RANGRF and explore its potential regulatory mechanism in arrhythmogenesis. METHODS: Based on bioinformatic analysis, miR-3144-5p was predicted to be a regulatory miRNA of RANGRF, which were then validated through a dual-luciferase reporter plasmid assay. Subsequently, the expression level of miR-3144-5p in human cardiac myocytes (HCMs) was detected, followed by cell transfection with miR-3144-5p mimics. Transcriptome sequencing was then performed in HCMs with or without transfection. The sequencing results were subjected to bioinformatic analyses, including differentially expressed gene (DEG) analysis, functional enrichment analysis, protein-protein interaction (PPI) network analysis, miRNA-target gene analysis, and miRNA-transcription factor (TF)-target gene coregulatory network analysis. RESULTS: There really existed a regulatory relation between miR-3144-5p and RANGRF. The expression level of miR-3144-5p was low in HCMs. After cell transfection, miR-3144-5p expression level significantly increased in HCMs. Bioinformatic analyses of the transcriptome sequencing results identified 300 upregulated and 271 downregulated DEGs between miR-3144-5p mimic and control group. The upregulated genes ISL1 and neuregulin 1 (NRG1) were significantly enriched in cardiac muscle cell myoblast differentiation (GO:0060379). CCL21 was one of the hub genes in the PPI network and also a target gene of miR-3144-5p. Moreover, the TF of v-Myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog (MYCN) was involved in the miR-3144-5p-TF-target gene coregulatory network and interacted with the target genes of miR-3144-5p. CONCLUSION: ISL1, NRG1, CCL21, and MYCN were differentially expressed in the miR-3144-5p mimic group, suggesting that miR-3144-5p overexpression plays a role in HCMs by regulating these genes and TF. This study may provide new insight into the mechanisms behind the progression of cardiac arrhythmia.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
MicroRNAs/biossíntese
Miócitos Cardíacos/metabolismo
Proteína ran de Ligação ao GTP/genética
[Mh] Termos MeSH secundário: Quimiocina CCL21/biossíntese
Perfilação da Expressão Gênica
Seres Humanos
Proteínas com Homeodomínio LIM/biossíntese
Proteína Proto-Oncogênica N-Myc/biossíntese
Neuregulina-1/biossíntese
Fatores de Transcrição/biossíntese
Transcriptoma
Regulação para Cima
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL21 protein, human); 0 (Chemokine CCL21); 0 (LIM-Homeodomain Proteins); 0 (MYCN protein, human); 0 (MicroRNAs); 0 (N-Myc Proto-Oncogene Protein); 0 (NRG1 protein, human); 0 (Neuregulin-1); 0 (Transcription Factors); 0 (insulin gene enhancer binding protein Isl-1); EC 3.6.1.- (RANGNRF protein, human); EC 3.6.5.2 (ran GTP-Binding Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007539


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[PMID]:28611158
[Au] Autor:Kozai M; Kubo Y; Katakai T; Kondo H; Kiyonari H; Schaeuble K; Luther SA; Ishimaru N; Ohigashi I; Takahama Y
[Ad] Endereço:Division of Experimental Immunology, Institute of Advanced Medical Sciences, University of Tokushima, Tokushima, Japan.
[Ti] Título:Essential role of CCL21 in establishment of central self-tolerance in T cells.
[So] Source:J Exp Med;214(7):1925-1935, 2017 Jul 03.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The chemokine receptor CCR7 directs T cell relocation into and within lymphoid organs, including the migration of developing thymocytes into the thymic medulla. However, how three functional CCR7 ligands in mouse, CCL19, CCL21Ser, and CCL21Leu, divide their roles in immune organs is unclear. By producing mice specifically deficient in CCL21Ser, we show that CCL21Ser is essential for the accumulation of positively selected thymocytes in the thymic medulla. CCL21Ser-deficient mice were impaired in the medullary deletion of self-reactive thymocytes and developed autoimmune dacryoadenitis. T cell accumulation in the lymph nodes was also defective. These results indicate a nonredundant role of CCL21Ser in the establishment of self-tolerance in T cells in the thymic medulla, and reveal a functional inequality among CCR7 ligands in vivo.
[Mh] Termos MeSH primário: Tolerância Central/imunologia
Quimiocina CCL21/imunologia
Tolerância a Antígenos Próprios/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Doenças Autoimunes/genética
Doenças Autoimunes/imunologia
Doenças Autoimunes/metabolismo
Tolerância Central/genética
Quimiocina CCL21/genética
Quimiocina CCL21/metabolismo
Dacriocistite/genética
Dacriocistite/imunologia
Dacriocistite/metabolismo
Citometria de Fluxo
Expressão Gênica/imunologia
Linfonodos/imunologia
Linfonodos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Nus
Camundongos Transgênicos
Microscopia Confocal
Receptores CCR7/imunologia
Receptores CCR7/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Tolerância a Antígenos Próprios/genética
Linfócitos T/metabolismo
Timócitos/imunologia
Timócitos/metabolismo
Timo/imunologia
Timo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl21a protein, mouse); 0 (Ccr7 protein, mouse); 0 (Chemokine CCL21); 0 (Receptors, CCR7)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161864


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[PMID]:28339080
[Au] Autor:Zhang L; Xiao X; An H; Wang J; Ma Y; Qian YH
[Ad] Endereço:School of Basic Medical Sciences, Health Science Center, Xi'an Jiaotong University, Xi'an, Shanxi 710061, P.R. China.
[Ti] Título:Inhibition of CCR7 promotes NF-κB-dependent apoptosis and suppresses epithelial-mesenchymal transition in non-small cell lung cancer.
[So] Source:Oncol Rep;37(5):2913-2919, 2017 May.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Activation of C-C chemokine receptor type 7 (CCR7) has been demonstrated to mediate the occurrence and progression of non-small cell lung cancer (NSCLC). However, the potential therapeutic role of CCR7 inhibition in NSCLC is still obscure. Thus, the present study was conducted to investigate the molecular mechanism underlying the inhibition of CCR7 on cell apoptosis and epithelial-mesenchymal transition (EMT) in NSCLC A549 cells. Chemokine ligand 21 (CCL21) was used to activate CCR7 and the results revealed that CCR7 upregulation inhibited cell apoptosis and affected apoptosis­related protein levels. However, CCR7-siRNA treatment markedly promoted apoptosis and suppressed inflammatory response and transforming growth factor ß1 (TGF-ß1)-induced EMT. In addition, CCR7­siRNA inactivated the NF-κB signaling pathway and inhibition of NF-κB via its specific antagonist, pyrrolidine dithiocarbamate, indicated that NF-κB was involved in the CCR7-mediated apoptosis. In conclusion, upregulation of CCR7 promoted cell proliferation and inflammation in A549 cells. In conclusion, inhibition of CCR7 via siRNA treatment promoted cell apoptosis and suppressed the inflammatory response and TGF-ß1­induced EMT, which may be associated with NF-κB signaling.
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Células não Pequenas/metabolismo
Quimiocina CCL21/farmacologia
Neoplasias Pulmonares/metabolismo
NF-kappa B/metabolismo
Receptores CCR7/metabolismo
[Mh] Termos MeSH secundário: Células A549
Apoptose
Carcinoma Pulmonar de Células não Pequenas/genética
Transição Epitelial-Mesenquimal
Seres Humanos
Neoplasias Pulmonares/genética
RNA Interferente Pequeno/farmacologia
Receptores CCR7/genética
Transdução de Sinais
Fator de Crescimento Transformador beta1/farmacologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCR7 protein, human); 0 (Chemokine CCL21); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Receptors, CCR7); 0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.3892/or.2017.5524


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[PMID]:28284342
[Au] Autor:Nguyen T; Lagman C; Chung LK; Chen CH; Poon J; Ong V; Voth BL; Yang I
[Ad] Endereço:Department of Neurosurgery, University of California, Los Angeles, Los Angeles, CA, United States; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
[Ti] Título:Insights into CCL21's roles in immunosurveillance and immunotherapy for gliomas.
[So] Source:J Neuroimmunol;305:29-34, 2017 Apr 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chemokine (C-C) motif ligand 21 (CCL21) is involved in immunosurveillance and has recently garnered the attention of neuro-oncologists and neuroscientists. CCL21 contains an extended C-terminus, which increases binding to lymphatic glycosaminoglycans and provides a mechanism for cell trafficking by forming a stationary chemokine concentration gradient that allows cell migration via haptotaxis. CCL21 is expressed by endothelial cells of the blood-brain barrier in physiologic and pathologic conditions. CCL21 has also been implicated in leukocyte extravasation into the central nervous system. In this review, we summarize the role of CCL21 in immunosurveillance and explore its potential as an immunotherapeutic agent for the treatment of gliomas.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/imunologia
Neoplasias Encefálicas/terapia
Quimiocina CCL21/uso terapêutico
Glioma/imunologia
Glioma/terapia
Imunoterapia/métodos
Monitorização Imunológica
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CCL21 protein, human); 0 (Chemokine CCL21)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


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[PMID]:28267881
[Au] Autor:Penteado LA; Dejani NN; Verdan FF; Orlando AB; Niño VE; Dias FN; Salina ACG; Medeiros AI
[Ad] Endereço:Department of Biological Sciences, School of Pharmaceutical Sciences, São Paulo State University (UNESP), Araraquara, São Paulo, Brazil.
[Ti] Título:Distinctive role of efferocytosis in dendritic cell maturation and migration in sterile or infectious conditions.
[So] Source:Immunology;151(3):304-313, 2017 Jul.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Efferocytosis, or clearance of apoptotic cells (ACs), by dendritic cells (DCs) leads to immune response suppression and tolerance to self-antigens. However, efferocytosis of infected apoptotic cells (IACs) leads to the production of a mixed pro- and anti-inflammatory cytokine milieu. We examined the DC phenotype and ability to migrate after phagocytosis of ACs or IACs and observed higher levels of CD86 and CCR7 expression in DCs, as well as enhanced migration capacity following efferocytosis of IACs. Interestingly, higher levels of interleukin-1ß, interleukin-10 and prostaglandin E (PGE ) were also produced in this context. Blockage of IAC recognition led to an impaired maturation profile and PGE production, which may have contributed to reduced CD86 and CCR7 expression and migration capacity. These data contribute to the understanding of how efferocytosis of sterile or infected cells may regulate the adaptive immune response, although the precise role of PGE in this process requires further investigation.
[Mh] Termos MeSH primário: Apoptose
Quimiotaxia
Células Dendríticas/patologia
Infecções por Escherichia coli/patologia
Linfonodos/patologia
Macrófagos/patologia
Fagocitose
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/metabolismo
Quimiocina CCL19/metabolismo
Quimiocina CCL21/metabolismo
Técnicas de Cocultura
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Células Dendríticas/microbiologia
Dinoprostona/metabolismo
Infecções por Escherichia coli/imunologia
Infecções por Escherichia coli/metabolismo
Infecções por Escherichia coli/microbiologia
Feminino
Mediadores da Inflamação/metabolismo
Linfonodos/imunologia
Linfonodos/metabolismo
Macrófagos/imunologia
Macrófagos/metabolismo
Macrófagos/microbiologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Fenótipo
Células RAW 264.7
Receptores CCR7/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (Ccl19 protein, mouse); 0 (Ccr7 protein, mouse); 0 (Cd86 protein, mouse); 0 (Chemokine CCL19); 0 (Chemokine CCL21); 0 (Inflammation Mediators); 0 (Receptors, CCR7); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12731


  9 / 683 MEDLINE  
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[PMID]:28087664
[Au] Autor:Yin X; Yu H; Jin X; Li J; Guo H; Shi Q; Yin Z; Xu Y; Wang X; Liu R; Wang S; Zhang L
[Ad] Endereço:Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
[Ti] Título:Human Blood CD1c+ Dendritic Cells Encompass CD5high and CD5low Subsets That Differ Significantly in Phenotype, Gene Expression, and Functions.
[So] Source:J Immunol;198(4):1553-1564, 2017 Feb 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There are three major dendritic cell (DC) subsets in both humans and mice, that is, plasmacytoid DCs and two types of conventional DCs (cDCs), cDC1s and cDC2s. cDC2s are important for polarizing CD4 naive T cells into different subsets, including Th1, Th2, Th17, Th22, and regulatory T cells. In mice, cDC2s can be further divided into phenotypically and functionally distinct subgroups. However, subsets of human cDC2s have not been reported. In the present study, we showed that human blood CD1c cDCs (cDC2s) can be further separated into two subpopulations according to their CD5 expression status. Comparative transcriptome analyses showed that the CD5 DCs expressed higher levels of cDC2-specific genes, including IFN regulatory factor 4, which is essential for the cDC2 development and its migration to lymph nodes. In contrast, CD5 DCs preferentially expressed monocyte-related genes, including the lineage-specific transcription factor MAFB. Furthermore, compared with the CD5 subpopulation, the CD5 subpopulation showed stronger migration toward CCL21 and overrepresentation among migratory DCs in lymph nodes. Additionally, the CD5 DCs induced naive T cell proliferation more potently than did the CD5 DCs. Moreover, CD5 DCs induced higher levels of IL-10-, IL-22-, and IL-4-producing T cell formation, whereas CD5 DCs induced higher levels of IFN-γ-producing T cell formation. Thus, we show that human blood CD1c cDC2s encompass two subsets that differ significantly in phenotype, that is, gene expression and functions. We propose that these two subsets of human cDC2s could potentially play contrasting roles in immunity or tolerance.
[Mh] Termos MeSH primário: Antígenos CD1/imunologia
Antígenos CD5/genética
Células Dendríticas/imunologia
Células Dendríticas/fisiologia
Glicoproteínas/imunologia
[Mh] Termos MeSH secundário: Antígenos CD1/genética
Células Sanguíneas/imunologia
Antígenos CD5/análise
Diferenciação Celular/efeitos dos fármacos
Quimiocina CCL21/farmacologia
Células Dendríticas/classificação
Células Dendríticas/efeitos dos fármacos
Glicoproteínas/genética
Seres Humanos
Tolerância Imunológica
Fatores Reguladores de Interferon/genética
Fatores Reguladores de Interferon/imunologia
Interleucina-10/imunologia
Interleucina-4/biossíntese
Interleucina-4/imunologia
Interleucinas/biossíntese
Interleucinas/imunologia
Ativação Linfocitária
Fenótipo
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Reguladores/imunologia
Células Th1/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD1); 0 (CCL21 protein, human); 0 (CD1C protein, human); 0 (CD5 Antigens); 0 (Chemokine CCL21); 0 (Glycoproteins); 0 (IL10 protein, human); 0 (Interferon Regulatory Factors); 0 (Interleukins); 0 (interferon regulatory factor-4); 0 (interleukin-22); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600193


  10 / 683 MEDLINE  
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[PMID]:28082403
[Au] Autor:Irshad S; Flores-Borja F; Lawler K; Monypenny J; Evans R; Male V; Gordon P; Cheung A; Gazinska P; Noor F; Wong F; Grigoriadis A; Fruhwirth GO; Barber PR; Woodman N; Patel D; Rodriguez-Justo M; Owen J; Martin SG; Pinder SE; Gillett CE; Poland SP; Ameer-Beg S; McCaughan F; Carlin LM; Hasan U; Withers DR; Lane P; Vojnovic B; Quezada SA; Ellis P; Tutt AN; Ng T
[Ad] Endereço:Breast Cancer Now (BCN) Research Unit, King's College London, London, United Kingdom.
[Ti] Título:RORγt Innate Lymphoid Cells Promote Lymph Node Metastasis of Breast Cancers.
[So] Source:Cancer Res;77(5):1083-1096, 2017 Mar 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cells tend to metastasize first to tumor-draining lymph nodes, but the mechanisms mediating cancer cell invasion into the lymphatic vasculature remain little understood. Here, we show that in the human breast tumor microenvironment (TME), the presence of increased numbers of RORγt group 3 innate lymphoid cells (ILC3) correlates with an increased likelihood of lymph node metastasis. In a preclinical mouse model of breast cancer, CCL21-mediated recruitment of ILC3 to tumors stimulated the production of the CXCL13 by TME stromal cells, which in turn promoted ILC3-stromal interactions and production of the cancer cell motile factor RANKL. Depleting ILC3 or neutralizing CCL21, CXCL13, or RANKL was sufficient to decrease lymph node metastasis. Our findings establish a role for RORγt ILC3 in promoting lymphatic metastasis by modulating the local chemokine milieu of cancer cells in the TME. .
[Mh] Termos MeSH primário: Neoplasias da Mama/imunologia
Neoplasias da Mama/patologia
Linfócitos/imunologia
Linfócitos/patologia
Receptores Nucleares Órfãos/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Quimiocina CCL21/imunologia
Quimiocina CXCL13/imunologia
Feminino
Seres Humanos
Imunidade Inata
Metástase Linfática
Neoplasias Mamárias Experimentais/imunologia
Neoplasias Mamárias Experimentais/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Transgênicos
Metástase Neoplásica
Neoplasias de Mama Triplo Negativas/imunologia
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL21); 0 (Chemokine CXCL13); 0 (Orphan Nuclear Receptors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-0598



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