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[PMID]:27776600
[Au] Autor:Petrone L; Cannas A; Vanini V; Cuzzi G; Aloi F; Nsubuga M; Sserunkuma J; Nazziwa RA; Jugheli L; Lukindo T; Girardi E; Antinori A; Pucci L; Reither K; Goletti D
[Ad] Endereço:Translational Research Unit, Department of Epidemiology and Preclinical Research, National Institute for Infectious Diseases (INMI), Rome, Italy.
[Ti] Título:Blood and urine inducible protein 10 as potential markers of disease activity.
[So] Source:Int J Tuberc Lung Dis;20(11):1554-1561, 2016 Nov.
[Is] ISSN:1815-7920
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:SETTING: Blood interferon-γ inducible protein 10 (IP-10) has been proposed as a biomarker of disease activity for both tuberculosis (TB) and human immunodeficiency virus (HIV) infection. Urine IP-10 has been detected in adults with active TB, and its level decreases after successful anti-tuberculosis treatment. OBJECTIVE: To evaluate blood and urine IP-10 as biomarker of disease activity. DESIGN: Patients with HIV-TB and active TB were enrolled. Individuals with HIV infection only and healthy donors were included as controls. Blood and urine IP-10 levels were measured using an enzyme-linked immunosorbent assay. RESULTS: Of 39 active TB patients enrolled, 24 were HIV-infected and 15 were HIV-uninfected. Of 87 control subjects without active TB, 54 were HIV-infected and 33 were HIV-uninfected. IP-10 analysis was performed in patients with concomitant blood and urine sample collection. Blood IP-10 was associated with active TB, regardless of HIV infection status; urine IP-10 levels were increased in active TB patients, although the difference was significant in HIV-infected individuals only. Finally, in HIV-infected patients, both blood and urine IP-10 levels were inversely correlated with CD4 T-cell counts. CONCLUSION: These findings suggest that IP-10 could be used as a biomarker for disease activity (inflammation).
[Mh] Termos MeSH primário: Quimiocina CXCL10/sangue
Quimiocina CXCL10/urina
Infecções por HIV/diagnóstico
Tuberculose/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/sangue
Biomarcadores/urina
Contagem de Linfócito CD4
Estudos Transversais
Ensaio de Imunoadsorção Enzimática
Feminino
Infecções por HIV/sangue
Infecções por HIV/urina
Seres Humanos
Interferon gama/sangue
Interleucina-6/sangue
Masculino
Meia-Idade
Tuberculose/sangue
Tuberculose/urina
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CXCL10 protein, human); 0 (Chemokine CXCL10); 0 (IFNG protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 82115-62-6 (Interferon-gamma)
[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:161026
[St] Status:MEDLINE


  2 / 2808 MEDLINE  
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[PMID]:29207310
[Au] Autor:Tokunaga R; Zhang W; Naseem M; Puccini A; Berger MD; Soni S; McSkane M; Baba H; Lenz HJ
[Ad] Endereço:Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA 90033, United States.
[Ti] Título:CXCL9, CXCL10, CXCL11/CXCR3 axis for immune activation - A target for novel cancer therapy.
[So] Source:Cancer Treat Rev;63:40-47, 2018 Feb.
[Is] ISSN:1532-1967
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chemokines are proteins which induce chemotaxis, promote differentiation of immune cells, and cause tissue extravasation. Given these properties, their role in anti-tumor immune response in the cancer environment is of great interest. Although immunotherapy has shown clinical benefit for some cancer patients, other patients do not respond. One of the mechanisms of resistance to checkpoint inhibitors may be chemokine signaling. The CXCL9, -10, -11/CXCR3 axis regulates immune cell migration, differentiation, and activation, leading to tumor suppression (paracrine axis). However, there are some reports that show involvements of this axis in tumor growth and metastasis (autocrine axis). Thus, a better understanding of CXCL9, -10, -11/CXCR3 axis is necessary to develop effective cancer control. In this article, we summarize recent evidence regarding CXCL9, CXCL10, CXCL11/CXCR3 axis in the immune system and discuss their potential role in cancer treatment.
[Mh] Termos MeSH primário: Quimiocina CXCL10/imunologia
Quimiocina CXCL11/imunologia
Quimiocina CXCL9/imunologia
Ativação Linfocitária/imunologia
Neoplasias/imunologia
Receptores CXCR3/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chemokine CXCL10); 0 (Chemokine CXCL11); 0 (Chemokine CXCL9); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


  3 / 2808 MEDLINE  
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[PMID]:29187588
[Au] Autor:Alanio C; Barreira da Silva R; Michonneau D; Bousso P; Ingersoll MA; Albert ML
[Ad] Endereço:Laboratory of Dendritic Cell Immunology, Institut Pasteur, 75015 Paris, France.
[Ti] Título:CXCR3/CXCL10 Axis Shapes Tissue Distribution of Memory Phenotype CD8 T Cells in Nonimmunized Mice.
[So] Source:J Immunol;200(1):139-146, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The preimmune repertoire consists of mature T lymphocytes that have not yet been stimulated in the periphery. Memory phenotype (MP) cells have been reported as part of the preimmune repertoire (i.e., T cells bearing memory markers despite lack of engagement with cognate Ag); however, little is known about their trafficking and function. In this study, we hypothesized that MP cells, naive to TCR stimulation, constitute a transient population that traffics to tissues during development. Using mutant and transgenic animals with a monospecific TCR, we discovered increased numbers of MP CD8 T cells circulating in nonimmunized and mice compared with wild-type animals. Phenotypic differences included decreased numbers of preimmune MP Ag-specific T cells in the skin and thymus and a distinct pattern of activation upon TCR engagement. Our results show for the first time, to our knowledge, an important role for CXCR3 and CXCL10 in the tissue distribution of preimmune MP cells.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Quimiocina CXCL10/metabolismo
Receptores CXCR3/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Quimiocina CXCL10/genética
Quimiocina CXCL9/genética
Quimiocina CXCL9/metabolismo
Memória Imunológica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Receptores de Antígenos de Linfócitos T/metabolismo
Receptores CXCR3/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokine CXCL10); 0 (Chemokine CXCL9); 0 (Cxcr3 protein, mouse); 0 (Receptors, Antigen, T-Cell); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700564


  4 / 2808 MEDLINE  
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[PMID]:28471454
[Au] Autor:Gao J; Fan M; Xiang G; Wang J; Zhang X; Guo W; Wu X; Sun Y; Gu Y; Ge H; Tan R; Qiu H; Shen Y; Xu Q
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, China.
[Ti] Título:Diptoindonesin G promotes ERK-mediated nuclear translocation of p-STAT1 (Ser727) and cell differentiation in AML cells.
[So] Source:Cell Death Dis;8(5):e2765, 2017 May 04.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Exploration of a new differentiation therapy that extends the range of differentiation for treating acute myeloid leukemia (AML) is attractive to researchers and clinicians. Here we report that diptoindonesin G (Dip G), a natural resveratrol aneuploid, exerts antiproliferative activity by inducing G2/M phase arrest and cell differentiation in AML cell lines and primary AML cells. Gene-profiling experiments showed that treating human leukemia HL-60 cells with Dip G was associated with a remarkable upregulation of STAT1 target gene expression, including IFIT3 and CXCL10. Mechanistically, Dip G activated ERK, which caused phosphorylation of STAT1 at Ser727 and selectively enhanced the interaction of p-STAT1 (Ser727) and p-ERK, further promoting their nuclear translocation. The nuclear translocation of p-STAT1 and p-ERK enhanced the transactivation of STAT1-targeted genes in AML cells. Furthermore, in vivo treatment of HL-60 xenografts demonstrated that Dip G significantly inhibited tumor growth and reduced tumor weight by inducing cell differentiation. Taken together, these results shed light on an essential role for ERK-mediated nuclear translocation of p-STAT1 (Ser727) and its full transcriptional activity in Dip G-induced differentiation of AML cells. Furthermore, these results demonstrate that Dip G could be used as a differentiation-inducing agent for AML therapy, particularly for non-acute promyelocytic leukemia therapy.
[Mh] Termos MeSH primário: Benzofuranos/farmacologia
Diferenciação Celular/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Fator de Transcrição STAT1/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Antineoplásicos/toxicidade
Benzofuranos/uso terapêutico
Caspase 3/química
Caspase 3/metabolismo
Inibidores de Caspase/farmacologia
Linhagem Celular Tumoral
Núcleo Celular/metabolismo
Proliferação Celular/efeitos dos fármacos
Quimiocina CXCL10/metabolismo
Células HL-60
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/metabolismo
Leucemia Mieloide Aguda/patologia
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Fosforilação/efeitos dos fármacos
Fator de Transcrição STAT1/genética
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Benzofurans); 0 (Caspase Inhibitors); 0 (Chemokine CXCL10); 0 (IFIT3 protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (STAT1 Transcription Factor); 0 (diptoindonesin G); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2017.159


  5 / 2808 MEDLINE  
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[PMID]:28468883
[Au] Autor:Srivastava R; Khan AA; Chilukuri S; Syed SA; Tran TT; Furness J; Bahraoui E; BenMohamed L
[Ad] Endereço:Laboratory of Cellular and Molecular Immunology, Gavin Herbert Eye Institute, University of California Irvine, School of Medicine, Irvine, California, USA.
[Ti] Título:CXCL10/CXCR3-Dependent Mobilization of Herpes Simplex Virus-Specific CD8 T and CD8 T Cells within Infected Tissues Allows Efficient Protection against Recurrent Herpesvirus Infection and Disease.
[So] Source:J Virol;91(14), 2017 Jul 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpes simplex virus 1 (HSV-1) establishes latency within the sensory neurons of the trigeminal ganglia (TG). HSV-specific memory CD8 T cells play a critical role in preventing HSV-1 reactivation from TG and subsequent virus shedding in tears that trigger recurrent corneal herpetic disease. The CXC chemokine ligand 10 (CXCL10)/CXC chemokine receptor 3 (CXCR3) chemokine pathway promotes T cell immunity to many viral pathogens, but its importance in CD8 T cell immunity to recurrent herpes has been poorly elucidated. In this study, we determined how the CXCL10/CXCR3 pathway affects TG- and cornea-resident CD8 T cell responses to recurrent ocular herpesvirus infection and disease using a well-established murine model in which HSV-1 reactivation was induced from latently infected TG by UV-B light. Following UV-B-induced HSV-1 reactivation, a significant increase in both the number and function of HSV-specific CXCR3 CD8 T cells was detected in TG and corneas of protected C57BL/6 (B6) mice, but not in TG and corneas of nonprotected CXCL10 or CXCR3 deficient mice. This increase was associated with a significant reduction in both virus shedding and recurrent corneal herpetic disease. Furthermore, delivery of exogenous CXCL10 chemokine in TG of CXCL10 mice, using the neurotropic adeno-associated virus type 8 (AAV8) vector, boosted the number and function of effector memory CD8 T cells (T ) and tissue-resident memory CD8 T cells (T ), but not of central memory CD8 T cells (T ), locally within TG, and improved protection against recurrent herpesvirus infection and disease in CXCL10 deficient mice. These findings demonstrate that the CXCL10/CXCR3 chemokine pathway is critical in shaping CD8 T cell immunity, locally within latently infected tissues, which protects against recurrent herpesvirus infection and disease. We determined how the CXCL10/CXCR3 pathway affects CD8 T cell responses to recurrent ocular herpesvirus infection and disease. Using a well-established murine model, in which HSV-1 reactivation in latently infected trigeminal ganglia was induced by UV-B light, we demonstrated that lack of either CXCL10 chemokine or its CXCR3 receptor compromised the mobilization of functional CD8 T and CD8 T cells within latently infected trigeminal ganglia following virus reactivation. This lack of T cell mobilization was associated with an increase in recurrent ocular herpesvirus infection and disease. Inversely, augmenting the amount of CXCL10 in trigeminal ganglia of latently infected CXCL10-deficient mice significantly restored the number of local antiviral CD8 T and CD8 T cells associated with protection against recurrent ocular herpes. Based on these findings, a novel "prime/pull" therapeutic ocular herpes vaccine strategy is proposed and discussed.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Quimiocina CXCL10/metabolismo
Herpes Simples/imunologia
Memória Imunológica
Receptores CXCR3/metabolismo
Simplexvirus/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL10/deficiência
Córnea/imunologia
Córnea/virologia
Modelos Animais de Doenças
Herpes Simples/prevenção & controle
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores CXCR3/deficiência
Recidiva
Gânglio Trigeminal/imunologia
Gânglio Trigeminal/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL10); 0 (Cxcl10 protein, mouse); 0 (Cxcr3 protein, mouse); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  6 / 2808 MEDLINE  
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[PMID]:29017920
[Au] Autor:Cho J; Yi H; Jang EY; Lee MS; Lee JY; Kang C; Lee CH; Kim K
[Ad] Endereço:Division of Viral Disease Research, Center for Infectious Diseases Research, Korea National Institute of Health, Cheongju, Republic of Korea; Department of Microbiology, Chungbuk National University, Cheongju, Republic of Korea.
[Ti] Título:Mycophenolic mofetil, an alternative antiviral and immunomodulator for the highly pathogenic avian influenza H5N1 virus infection.
[So] Source:Biochem Biophys Res Commun;494(1-2):298-304, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection with the highly pathogenic avian influenza H5N1 virus results in a high incidence of mortality in humans. Severe complications from infection are often associated with hypercytokinemia. However, current neuraminidase inhibitors (NAIs) have several limitations including the appearance of oseltamivir-resistant H5N1 virus and the inability to completely ameliorate hyper-immune responses. To overcome these limitations, we evaluated the anti-viral activity of mycophenolic mofetil (MMF) against A/Vietnam/1194/2004 (H5N1) virus infection using MDCK cells and mice. The IC of MMF (0.94 µM) was comparable to that of zanamivir (0.87 µM) in H5N1 virus-infected MDCK cells based on ELISA. Time-course assays demonstrated that MMF completely inhibited H5N1 viral mRNA replication and protein expression for approximately 8 h after the initiation of treatment. In addition, MMF treatment protected 100% of mice, and lung viral titers were substantially reduced. The anti-viral mechanism of MMF against H5N1 virus infection was further confirmed to depend on the inhibition of cellular inosine monophosphate dehydrogenase (IMPDH) by exogenous guanosine, which inhibits viral mRNA and protein expression. Moreover, IL-1ß, IFN-ß, IL-6, and IP-10 mRNA expression levels were significantly downregulated in MDCK cells with MMF treatment. These results indicated that MMF could represent a novel inhibitor of viral replication and a potent immunomodulator for the treatment of H5N1 virus infection.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Fatores Imunológicos/farmacologia
Vírus da Influenza A Subtipo H5N1/efeitos dos fármacos
Ácido Micofenólico/farmacologia
Infecções por Orthomyxoviridae/tratamento farmacológico
Oseltamivir/farmacologia
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL10/antagonistas & inibidores
Quimiocina CXCL10/genética
Quimiocina CXCL10/imunologia
Embrião de Galinha
Cães
Feminino
Regulação da Expressão Gênica
Interações Hospedeiro-Patógeno/efeitos dos fármacos
IMP Desidrogenase/antagonistas & inibidores
IMP Desidrogenase/genética
IMP Desidrogenase/imunologia
Vírus da Influenza A Subtipo H5N1/crescimento & desenvolvimento
Vírus da Influenza A Subtipo H5N1/patogenicidade
Interferon beta/antagonistas & inibidores
Interferon beta/genética
Interferon beta/imunologia
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/genética
Interleucina-1beta/imunologia
Interleucina-6/antagonistas & inibidores
Interleucina-6/genética
Interleucina-6/imunologia
Pulmão/efeitos dos fármacos
Pulmão/imunologia
Pulmão/virologia
Células Madin Darby de Rim Canino
Camundongos
Camundongos Endogâmicos BALB C
Infecções por Orthomyxoviridae/imunologia
Infecções por Orthomyxoviridae/mortalidade
Infecções por Orthomyxoviridae/patologia
RNA Viral/antagonistas & inibidores
RNA Viral/biossíntese
Análise de Sobrevida
Replicação Viral/efeitos dos fármacos
Zanamivir/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Chemokine CXCL10); 0 (Cxcl10 protein, mouse); 0 (IL1B protein, mouse); 0 (Immunologic Factors); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (RNA, Viral); 0 (interleukin-6, mouse); 20O93L6F9H (Oseltamivir); 77238-31-4 (Interferon-beta); EC 1.1.1.205 (IMP Dehydrogenase); HU9DX48N0T (Mycophenolic Acid); L6O3XI777I (Zanamivir)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE


  7 / 2808 MEDLINE  
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[PMID]:28904072
[Au] Autor:Srugo I; Klein A; Stein M; Golan-Shany O; Kerem N; Chistyakov I; Genizi J; Glazer O; Yaniv L; German A; Miron D; Shachor-Meyouhas Y; Bamberger E; Oved K; Gottlieb TM; Navon R; Paz M; Etshtein L; Boico O; Kronenfeld G; Eden E; Cohen R; Chappuy H; Angoulvant F; Lacroix L; Gervaix A
[Ad] Endereço:Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel; isaac.srugo@b-zion.org.il.
[Ti] Título:Validation of a Novel Assay to Distinguish Bacterial and Viral Infections.
[So] Source:Pediatrics;140(4), 2017 Oct.
[Is] ISSN:1098-4275
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Reliably distinguishing bacterial from viral infections is often challenging, leading to antibiotic misuse. A novel assay that integrates measurements of blood-borne host-proteins (tumor necrosis factor-related apoptosis-inducing ligand, interferon γ-induced protein-10, and C-reactive protein [CRP]) was developed to assist in differentiation between bacterial and viral disease. METHODS: We performed double-blind, multicenter assay evaluation using serum remnants collected at 5 pediatric emergency departments and 2 wards from children ≥3 months to ≤18 years without ( = 68) and with ( = 529) suspicion of acute infection. Infectious cohort inclusion criteria were fever ≥38°C and symptom duration ≤7 days. The reference standard diagnosis was based on predetermined criteria plus adjudication by experts blinded to assay results. Assay performers were blinded to the reference standard. Assay cutoffs were predefined. RESULTS: Of 529 potentially eligible patients with suspected acute infection, 100 did not fulfill infectious inclusion criteria and 68 had insufficient serum. The resulting cohort included 361 patients, with 239 viral, 68 bacterial, and 54 indeterminate reference standard diagnoses. The assay distinguished between bacterial and viral patients with 93.8% sensitivity (95% confidence interval: 87.8%-99.8%) and 89.8% specificity (85.6%-94.0%); 11.7% had an equivocal assay outcome. The assay outperformed CRP (cutoff 40 mg/L; sensitivity 88.2% [80.4%-96.1%], specificity 73.2% [67.6%-78.9%]) and procalcitonin testing (cutoff 0.5 ng/mL; sensitivity 63.1% [51.0%-75.1%], specificity 82.3% [77.1%-87.5%]). CONCLUSIONS: Double-blinded evaluation confirmed high assay performance in febrile children. Assay was significantly more accurate than CRP, procalcitonin, and routine laboratory parameters. Additional studies are warranted to support its potential to improve antimicrobial treatment decisions.
[Mh] Termos MeSH primário: Infecções Bacterianas/diagnóstico
Proteína C-Reativa/metabolismo
Quimiocina CXCL10/sangue
Ligante Indutor de Apoptose Relacionado a TNF/sangue
Viroses/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Infecções Bacterianas/sangue
Biomarcadores/sangue
Criança
Pré-Escolar
Diagnóstico Diferencial
Método Duplo-Cego
Feminino
Seres Humanos
Lactente
Masculino
Estudos Prospectivos
Sensibilidade e Especificidade
Viroses/sangue
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; MULTICENTER STUDY; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Biomarkers); 0 (CXCL10 protein, human); 0 (Chemokine CXCL10); 0 (TNF-Related Apoptosis-Inducing Ligand); 0 (TNFSF10 protein, human); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171112
[Lr] Data última revisão:
171112
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE


  8 / 2808 MEDLINE  
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[PMID]:28899907
[Au] Autor:Zhao Q; Kim T; Pang J; Sun W; Yang X; Wang J; Song Y; Zhang H; Sun H; Rangan V; Deshpande S; Tang H; Cvijic ME; Westhouse R; Olah T; Xie J; Struthers M; Salter-Cid L
[Ad] Endereço:Discovery Biology, Immuno-Science, Bristol Myers Squibb, Princeton, New Jersey, USA; qihong.zhao@bms.com.
[Ti] Título:A novel function of CXCL10 in mediating monocyte production of proinflammatory cytokines.
[So] Source:J Leukoc Biol;102(5):1271-1280, 2017 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IFN-γ-inducible protein 10 (CXCL10), a chemokine that is abundantly secreted in response to inflammatory stimuli, has been implicated in the pathogenesis of multiple inflammatory diseases, such as inflammatory bowel disease. Whereas CXCL10 is traditionally recognized for recruiting pathogenic T cells to inflamed sites, its nonchemotactic role during inflammation remains poorly defined. In this report, we identified a novel function of CXCL10 in the regulation of the inflammatory potential of human monocytes to produce cytokines. We found that CXCL10 was necessary and sufficient for IFN-γ-primed human monocytes to induce a robust production of proinflammatory cytokines, such as IL-12 and IL-23. CXCL10-induced monocyte production of these cytokines depended on CXCR3 receptor engagement as well as on the Iκ B kinase and p38 MAPK signaling pathways. By using an innate-mediated murine colitis model, we demonstrated that anti-CXCL10 Ab treatment robustly suppressed the local production of myeloid-derived inflammatory cytokines and intestinal tissue damage. Together, our data unravel a previously unappreciated role of CXCL10 in the amplification of myeloid cell-mediated inflammatory responses. Targeting CXCL10 is therefore an attractive approach to treating inflammatory diseases that are driven by innate and adaptive immunity.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Quimiocina CXCL10/imunologia
Colite Ulcerativa/imunologia
Doença de Crohn/imunologia
Imunidade Inata
Monócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/administração & dosagem
Antígenos CD40/antagonistas & inibidores
Quimiocina CXCL10/antagonistas & inibidores
Quimiocina CXCL10/genética
Colite/induzido quimicamente
Colite/genética
Colite/imunologia
Colite/patologia
Colite Ulcerativa/genética
Colite Ulcerativa/patologia
Doença de Crohn/genética
Doença de Crohn/patologia
Feminino
Regulação da Expressão Gênica
Seres Humanos
Quinase I-kappa B/genética
Quinase I-kappa B/imunologia
Interferon gama/genética
Interferon gama/imunologia
Interleucina-12/genética
Interleucina-12/imunologia
Interleucina-23/genética
Interleucina-23/imunologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Monócitos/citologia
Cultura Primária de Células
Receptores CXCR3/genética
Receptores CXCR3/imunologia
Transdução de Sinais
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (CD40 Antigens); 0 (Chemokine CXCL10); 0 (Cxcl10 protein, mouse); 0 (Cxcr3 protein, mouse); 0 (Interleukin-23); 0 (Receptors, CXCR3); 187348-17-0 (Interleukin-12); 82115-62-6 (Interferon-gamma); EC 2.7.11.10 (I-kappa B Kinase); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[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:170914
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.5A0717-302


  9 / 2808 MEDLINE  
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[PMID]:28859328
[Au] Autor:Rose T; Grützkau A; Klotsche J; Enghard P; Flechsig A; Keller J; Riemekasten G; Radbruch A; Burmester GR; Dörner T; Hiepe F; Biesen R
[Ad] Endereço:Department of Rheumatology and Clinical Immunology, Charité Universitätsmedizin Berlin.
[Ti] Título:Are interferon-related biomarkers advantageous for monitoring disease activity in systemic lupus erythematosus? A longitudinal benchmark study.
[So] Source:Rheumatology (Oxford);56(9):1618-1626, 2017 Sep 01.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objective: To determine the clinical value of six traditional and three IFN-related biomarkers in monitoring disease activity (DA) in SLE. Methods: Prospective longitudinal study of IFNα, IFNγ-inducible protein 10 (IP-10) and sialic acid-binding Ig-like lectin 1 (SIGLEC1) vs antibodies against dsDNA (ELISA and Farr radioimmunoassay), dsDNA-complexed nucleosomes (anti-dsDNA-NcX: ELISA), nucleosomes (ANuA: ELISA) and complement C3/C4 for correlation with DA (measured by BILAG 2004 index) in 26 SLE patients (77 visits). Optimal upper and lower longitudinal thresholds for the biomarkers and their accuracies for reflecting clinically relevant changes in DA (flares and remission) were determined by receiver operating characteristic and Youden index analysis. Results: Increases in IP-10, SIGLEC1 and ANuA to + 101.6 pg/ml, +5.01 relative mean fluorescence intensity and +16.20 IU/ml above the calculated upper longitudinal threshold significantly reflected lupus flares, with a sensitivity and specificity of 50 and 95% for IP-10, 83 and 90% for SIGLEC1 and 58 and 95% for ANuA. Decreases in anti-dsDNA (ELISA), IFNα and anti-dsDNA (Farr assay) to - 64.7 IU/ml, -16.69 pg/ml and -3.3 IU/ml below lower longitudinal thresholds, respectively, best reflected remission, with sensitivity and specificity of 75 and 95%, 62 and 90%, and 75 and 90%, respectively. Conclusion: IP-10, SIGLEC1 and ANuA emerged as advantageous biomarkers for monitoring disease activity. This is the first study in SLE that provides longitudinal biomarker thresholds and test accuracies for SLE flares and remitting disease. In the context of IFN-directed therapies, chemokines and fluorescence-activated cell sorting-based IFN biomarkers for monitoring SLE activity should be further studied.
[Mh] Termos MeSH primário: Interferon-alfa/sangue
Lúpus Eritematoso Sistêmico/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Idoso
Benchmarking
Biomarcadores/sangue
Quimiocina CXCL10/sangue
Feminino
Seres Humanos
Estudos Longitudinais
Masculino
Meia-Idade
Monócitos/metabolismo
Estudos Prospectivos
Sensibilidade e Especificidade
Índice de Gravidade de Doença
Lectina 1 Semelhante a Ig de Ligação ao Ácido Siálico/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CXCL10 protein, human); 0 (Chemokine CXCL10); 0 (Interferon-alpha); 0 (SIGLEC1 protein, human); 0 (Sialic Acid Binding Ig-like Lectin 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kex220


  10 / 2808 MEDLINE  
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[PMID]:28836736
[Au] Autor:Cédile O; Wlodarczyk A; Owens T
[Ad] Endereço:Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
[Ti] Título:CCL2 recruits T cells into the brain in a CCR2-independent manner.
[So] Source:APMIS;125(11):945-956, 2017 Nov.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:CCL2 is a chemokine that can be induced during neuroinflammation to recruit immune cells, but its role in the central nervous system (CNS) is unclear. Our aim was to better understand its role. We induced CCL2 in CNS of naive CCL2-deficient mice using intrathecally administered replication-defective adenovirus and examined cell infiltration by flow cytometry. CCL2 expression induced pronounced and unexpected recruitment of regulatory and IFNγ-producing T cells to CNS from blood, possibly related to defective egress of monocytes from CCL2-deficient bone marrow. Infiltration also occurred in mice lacking CCR2, a receptor for CCL2. Expression of another receptor for CCL2, CCR4, and CXCR3, a receptor for CXCL10, which was also induced, were both increased in CCL2-treated CNS. CCR4 was expressed by neurons and astrocytes as well as CD4 T cells, and CXCR3 was expressed by CD4 and CD8 T cells. Chemokine-recruited T cells did not lead to CNS pathology. Our findings show a role for CCL2 in recruitment of CD4 T cells to the CNS and show that redundancy among chemokine receptors ensures optimal response.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Sistema Nervoso Central/imunologia
Quimiocina CCL2/imunologia
Receptores CCR2/imunologia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Adenoviridae/metabolismo
Animais
Astrócitos/citologia
Astrócitos/imunologia
Linfócitos T CD4-Positivos/citologia
Linfócitos T CD8-Positivos/citologia
Movimento Celular
Sistema Nervoso Central/citologia
Quimiocina CCL2/deficiência
Quimiocina CCL2/genética
Quimiocina CXCL10/genética
Quimiocina CXCL10/imunologia
Feminino
Regulação da Expressão Gênica
Genes Reporter
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Injeções Espinhais
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos
Camundongos Knockout
Neurônios/citologia
Neurônios/imunologia
Receptores CCR2/genética
Receptores CCR4/genética
Receptores CCR4/imunologia
Receptores CXCR3/genética
Receptores CXCR3/imunologia
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ccl2 protein, mouse); 0 (Ccr2 protein, mouse); 0 (Ccr4 protein, mouse); 0 (Chemokine CCL2); 0 (Chemokine CXCL10); 0 (Cxcl10 protein, mouse); 0 (Cxcr3 protein, mouse); 0 (Luminescent Proteins); 0 (Receptors, CCR2); 0 (Receptors, CCR4); 0 (Receptors, CXCR3); 0 (Recombinant Fusion Proteins); 0 (red fluorescent protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12740



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