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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


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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


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[PMID]:28891812
[Au] Autor:Koyanagi N; Imai T; Shindo K; Sato A; Fujii W; Ichinohe T; Takemura N; Kakuta S; Uematsu S; Kiyono H; Maruzuru Y; Arii J; Kato A; Kawaguchi Y
[Ad] Endereço:Division of Molecular Virology, Department of Microbiology and Immunology.
[Ti] Título:Herpes simplex virus-1 evasion of CD8+ T cell accumulation contributes to viral encephalitis.
[So] Source:J Clin Invest;127(10):3784-3795, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herpes simplex virus-1 (HSV-1) is the most common cause of sporadic viral encephalitis, which can be lethal or result in severe neurological defects even with antiviral therapy. While HSV-1 causes encephalitis in spite of HSV-1-specific humoral and cellular immunity, the mechanism by which HSV-1 evades the immune system in the central nervous system (CNS) remains unknown. Here we describe a strategy by which HSV-1 avoids immune targeting in the CNS. The HSV-1 UL13 kinase promotes evasion of HSV-1-specific CD8+ T cell accumulation in infection sites by downregulating expression of the CD8+ T cell attractant chemokine CXCL9 in the CNS of infected mice, leading to increased HSV-1 mortality due to encephalitis. Direct injection of CXCL9 into the CNS infection site enhanced HSV-1-specific CD8+ T cell accumulation, leading to marked improvements in the survival of infected mice. This previously uncharacterized strategy for HSV-1 evasion of CD8+ T cell accumulation in the CNS has important implications for understanding the pathogenesis and clinical treatment of HSV-1 encephalitis.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Encefalite por Herpes Simples/imunologia
Herpesvirus Humano 1/imunologia
Evasão da Resposta Imune
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/patologia
Cercopithecus aethiops
Quimiocina CXCL9/genética
Quimiocina CXCL9/imunologia
Encefalite por Herpes Simples/genética
Encefalite por Herpes Simples/patologia
Herpesvirus Humano 1/genética
Imunidade Celular/genética
Camundongos
Camundongos Knockout
Proteínas Quinases/imunologia
Coelhos
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL9); 0 (Cxcl9 protein, mouse); EC 2.7.- (Protein Kinases); EC 2.7.1.- (UL13 protein, Simplexvirus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE


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[PMID]:28823882
[Au] Autor:Liu LY; Strassner JP; Refat MA; Harris JE; King BA
[Ad] Endereço:Yale University School of Medicine, New Haven, Connecticut.
[Ti] Título:Repigmentation in vitiligo using the Janus kinase inhibitor tofacitinib may require concomitant light exposure.
[So] Source:J Am Acad Dermatol;77(4):675-682.e1, 2017 Oct.
[Is] ISSN:1097-6787
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Vitiligo is an autoimmune disease in which cutaneous depigmentation occurs. Existing therapies are often inadequate. Prior reports have shown benefit of the Janus kinase (JAK) inhibitors. OBJECTIVE: To evaluate the efficacy of the JAK 1/3 inhibitor tofacitinib in the treatment of vitiligo. METHOD: This is a retrospective case series of 10 consecutive patients with vitiligo treated with tofacitinib. Severity of disease was assessed by body surface area of depigmentation. RESULTS: Ten consecutive patients were treated with tofacitinib. Five patients achieved some repigmentation at sites of either sunlight exposure or low-dose narrowband ultraviolet B phototherapy. Suction blister sampling revealed that the autoimmune response was inhibited during treatment in both responding and nonresponding lesions, suggesting that light rather than immunosuppression was primarily required for melanocyte regeneration. LIMITATIONS: Limitations include the small size of the study population, retrospective nature of the study, and lack of a control group. CONCLUSION: Treatment of vitiligo with JAK inhibitors appears to require light exposure. In contrast to treatment with phototherapy alone, repigmentation during treatment with JAK inhibitors may require only low-level light. Maintenance of repigmentation may be achieved with JAK inhibitor monotherapy. These results support a model wherein JAK inhibitors suppress T cell mediators of vitiligo and light exposure is necessary for stimulation of melanocyte regeneration.
[Mh] Termos MeSH primário: Piperidinas/uso terapêutico
Inibidores de Proteínas Quinases/uso terapêutico
Pirimidinas/uso terapêutico
Pirróis/uso terapêutico
Pigmentação da Pele
Terapia Ultravioleta
Vitiligo/terapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Autoimunidade
Quimiocina CXCL10/metabolismo
Quimiocina CXCL9/metabolismo
Terapia Combinada
Feminino
Seres Humanos
Janus Quinase 1/antagonistas & inibidores
Janus Quinase 3/antagonistas & inibidores
Masculino
Meia-Idade
Estudos Retrospectivos
Índice de Gravidade de Doença
Vitiligo/imunologia
Vitiligo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL10 protein, human); 0 (CXCL9 protein, human); 0 (Chemokine CXCL10); 0 (Chemokine CXCL9); 0 (Piperidines); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (Pyrroles); 87LA6FU830 (tofacitinib); EC 2.7.10.2 (Janus Kinase 1); EC 2.7.10.2 (Janus Kinase 3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE


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[PMID]:28760660
[Au] Autor:Ke Y; Dang E; Shen S; Zhang T; Qiao H; Chang Y; Liu Q; Wang G
[Ad] Endereço:Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China; Department of Oral Medicine, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi, China.
[Ti] Título:Semaphorin4D Drives CD8 T-Cell Lesional Trafficking in Oral Lichen Planus via CXCL9/CXCL10 Upregulations in Oral Keratinocytes.
[So] Source:J Invest Dermatol;137(11):2396-2406, 2017 Nov.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chemokine-mediated CD8 T-cell recruitment is an essential but not well-established event for the persistence of oral lichen planus (OLP). Semaphorin 4D (Sema4D)/CD100 is implicated in immune dysfunction, chemokine modulation, and cell migration, which are critical aspects for OLP progression, but its implication in OLP pathogenesis has not been determined. In this study, we sought to explicate the effect of Sema4D on human oral keratinocytes and its capacity to drive CD8 T-cell lesional trafficking via chemokine modulation. We found that upregulations of sSema4D in OLP tissues and blood were positively correlated with disease severity and activity. In vitro observation revealed that Sema4D induced C-X-C motif chemokine ligand 9/C-X-C motif chemokine ligand 10 production by binding to plexin-B1 via protein kinase B-NF-κB cascade in human oral keratinocytes, which elicited OLP CD8 T-cell migration. We also confirmed using clinical samples that elevated C-X-C motif chemokine ligand 9/C-X-C motif chemokine ligand 10 levels were positively correlated with sSema4D levels in OLP lesions and serum. Notably, we determined matrix metalloproteinase-9 as a new proteolytic enzyme for the cleavage of sSema4D from the T-cell surface, which may contribute to the high levels of sSema4D in OLP lesions and serum. Our findings conclusively revealed an amplification feedback loop involving T cells, chemokines, and Sema4D-dependent signal that promotes OLP progression.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Linfócitos T CD8-Positivos/metabolismo
Quimiocina CXCL10/genética
Quimiocina CXCL9/genética
Líquen Plano Bucal/genética
Líquen Plano Bucal/imunologia
Semaforinas/metabolismo
[Mh] Termos MeSH secundário: Administração Tópica
Doenças Autoimunes/genética
Doenças Autoimunes/imunologia
Biópsia por Agulha
Linfócitos T CD8-Positivos/imunologia
Estudos de Casos e Controles
Movimento Celular/genética
Células Cultivadas
Seres Humanos
Imuno-Histoquímica
Queratinócitos/metabolismo
Queratinócitos/patologia
Líquen Plano Bucal/tratamento farmacológico
Líquen Plano Bucal/patologia
RNA Interferente Pequeno/análise
Triancinolona/uso terapêutico
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD100 antigen); 0 (Chemokine CXCL10); 0 (Chemokine CXCL9); 0 (RNA, Small Interfering); 0 (Semaphorins); 1ZK20VI6TY (Triamcinolone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE


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[PMID]:28686641
[Au] Autor:Shino MY; Weigt SS; Li N; Palchevskiy V; Derhovanessian A; Saggar R; Sayah DM; Huynh RH; Gregson AL; Fishbein MC; Ardehali A; Ross DJ; Lynch JP; Elashoff RM; Belperio JA
[Ad] Endereço:Division of Pulmonary and Critical Care Medicine, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
[Ti] Título:The prognostic importance of CXCR3 chemokine during organizing pneumonia on the risk of chronic lung allograft dysfunction after lung transplantation.
[So] Source:PLoS One;12(7):e0180281, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Since the pathogenesis of chronic lung allograft dysfunction (CLAD) remains poorly defined with no known effective therapies, the identification and study of key events which increase CLAD risk is a critical step towards improving outcomes. We hypothesized that bronchoalveolar lavage fluid (BALF) CXCR3 ligand concentrations would be augmented during organizing pneumonia (OP) and that episodes of OP with marked chemokine elevations would be associated with significantly higher CLAD risk. METHODS: All transbronchial biopsies (TBBX) from patients who received lung transplantation between 2000 to 2010 were reviewed. BALF concentrations of the CXCR3 ligands (CXCL9, CXCL10 and CXCL11) were compared between episodes of OP and "healthy" biopsies using linear mixed-effects models. The association between CXCR3 ligand concentrations during OP and CLAD risk was evaluated using proportional hazards models with time-dependent covariates. RESULTS: There were 1894 bronchoscopies with TBBX evaluated from 441 lung transplant recipients with 169 (9%) episodes of OP and 907 (49%) non-OP histopathologic injuries. 62 (37%) episodes of OP were observed during routine surveillance bronchoscopy. Eight hundred thirty-eight (44%) TBBXs had no histopathology and were classified as "healthy" biopsies. There were marked elevations in BALF CXCR3 ligand concentrations during OP compared with "healthy" biopsies. In multivariable models adjusted for other injury patterns, OP did not significantly increase the risk of CLAD when BAL CXCR3 chemokine concentrations were not taken into account. However, OP with elevated CXCR3 ligands markedly increased CLAD risk in a dose-response manner. An episode of OP with CXCR3 concentrations greater than the 25th, 50th and 75th percentiles had HRs for CLAD of 1.5 (95% CI 1.0-2.3), 1.9 (95% CI 1.2-2.8) and 2.2 (95% CI 1.4-3.4), respectively. CONCLUSIONS: This study identifies OP, a relatively uncommon histopathologic finding after lung transplantation, as a major risk factor for CLAD development when considered in the context of increased allograft expression of interferon-γ inducible ELR- CXC chemokines. We further demonstrate for the first time, the prognostic importance of BALF CXCR3 ligand concentrations during OP on subsequent CLAD risk.
[Mh] Termos MeSH primário: Transplante de Pulmão
Pulmão/diagnóstico por imagem
Pulmão/fisiopatologia
Pneumonia/diagnóstico por imagem
Pneumonia/fisiopatologia
Receptores CXCR3/imunologia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores/química
Biomarcadores/metabolismo
Biópsia
Líquido da Lavagem Broncoalveolar/química
Líquido da Lavagem Broncoalveolar/imunologia
Broncoscopia
Quimiocina CXCL10/genética
Quimiocina CXCL10/imunologia
Quimiocina CXCL11/genética
Quimiocina CXCL11/imunologia
Quimiocina CXCL9/genética
Quimiocina CXCL9/imunologia
Feminino
Expressão Gênica
Seres Humanos
Ligantes
Pulmão/imunologia
Masculino
Meia-Idade
Pneumonia/genética
Pneumonia/imunologia
Modelos de Riscos Proporcionais
Receptores CXCR3/genética
Testes de Função Respiratória
Estudos Retrospectivos
Risco
Transplante Homólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CXCL10 protein, human); 0 (CXCL11 protein, human); 0 (CXCL9 protein, human); 0 (CXCR3 protein, human); 0 (Chemokine CXCL10); 0 (Chemokine CXCL11); 0 (Chemokine CXCL9); 0 (Ligands); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180281


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[PMID]:28578025
[Au] Autor:Fernández-Paredes L; Casrouge A; Decalf J; de Andrés C; Villar LM; Pérez de Diego R; Alonso B; Álvarez Cermeño JC; Arroyo R; Tejera-Alhambra M; Navarro J; Oreja-Guevara C; López Trascasa M; Seyfferth A; García Martínez MA; Álvarez Lafuente R; Albert ML; Sánchez-Ramón S
[Ad] Endereço:Dept. of Clinical Immunology and IdISSC, Hospital Clínico San Carlos, Madrid, Spain; Dept. of Microbiology I, Complutense University School of Medicine, Madrid, Spain.
[Ti] Título:Multimarker risk stratification approach at multiple sclerosis onset.
[So] Source:Clin Immunol;181:43-50, 2017 Aug.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Delay in the diagnosis of multiple sclerosis (MS) stems from the lack of specific clinical and analytical markers to assist in the early diagnosis and prediction of progressive course. We propose a decision-tree model that better defines early at onset MS patients and those with the progressive form by analysing a 12-biomarkers panel in serum and CSF samples of patients with MS, other neurological diseases (OND) and healthy contols. Thus, patients at onset of neurological disease were first classified by serum IL-7 levels <141pg/ml (OR=6.51, p<0.001). Combination of IL-7 and CXCL10 indicated risk for a specific MS clinical form, where IL-7<141 and CXCL10<570pg/ml were associated with the highest risk for PP-MS (OR=22, p=0.01). Unexpectedly, both PP-MS and RR-MS patients shared significantly decreased prototypical biomarkers of inflammation and tissue regeneration in CSF than OND suggesting a defective intrinsic immune response playing a role at the beginning of the disease.
[Mh] Termos MeSH primário: Esclerose Múltipla Crônica Progressiva/diagnóstico
Esclerose Múltipla Recidivante-Remitente/diagnóstico
[Mh] Termos MeSH secundário: Área Sob a Curva
Biomarcadores/sangue
Biomarcadores/líquido cefalorraquidiano
Estudos de Casos e Controles
Quimiocina CCL11
Quimiocina CCL2
Quimiocina CCL4
Quimiocina CCL5
Quimiocina CXCL10/sangue
Quimiocina CXCL10/líquido cefalorraquidiano
Quimiocina CXCL9/sangue
Quimiocina CXCL9/líquido cefalorraquidiano
Árvores de Decisões
Dipeptidil Peptidase 4/sangue
Dipeptidil Peptidase 4/líquido cefalorraquidiano
Diagnóstico Precoce
Fator de Crescimento Epidérmico
Fator 2 de Crescimento de Fibroblastos/sangue
Fator 2 de Crescimento de Fibroblastos/líquido cefalorraquidiano
Fator de Crescimento de Hepatócito
Seres Humanos
Proteína Antagonista do Receptor de Interleucina 1/sangue
Proteína Antagonista do Receptor de Interleucina 1/líquido cefalorraquidiano
Interleucina-7/sangue
Interleucina-7/líquido cefalorraquidiano
Esclerose Múltipla Crônica Progressiva/sangue
Esclerose Múltipla Crônica Progressiva/líquido cefalorraquidiano
Esclerose Múltipla Recidivante-Remitente/sangue
Esclerose Múltipla Recidivante-Remitente/líquido cefalorraquidiano
Análise Multivariada
Doenças do Sistema Nervoso/sangue
Doenças do Sistema Nervoso/líquido cefalorraquidiano
Doenças do Sistema Nervoso/diagnóstico
Prognóstico
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CCL11 protein, human); 0 (CCL2 protein, human); 0 (CCL4 protein, human); 0 (CCL5 protein, human); 0 (CXCL10 protein, human); 0 (CXCL9 protein, human); 0 (Chemokine CCL11); 0 (Chemokine CCL2); 0 (Chemokine CCL4); 0 (Chemokine CCL5); 0 (Chemokine CXCL10); 0 (Chemokine CXCL9); 0 (HGF protein, human); 0 (IL1RN protein, human); 0 (IL7 protein, human); 0 (Interleukin 1 Receptor Antagonist Protein); 0 (Interleukin-7); 103107-01-3 (Fibroblast Growth Factor 2); 62229-50-9 (Epidermal Growth Factor); 67256-21-7 (Hepatocyte Growth Factor); EC 3.4.14.5 (DPP4 protein, human); EC 3.4.14.5 (Dipeptidyl Peptidase 4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170605
[St] Status:MEDLINE


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[PMID]:28486109
[Au] Autor:Spranger S; Dai D; Horton B; Gajewski TF
[Ad] Endereço:Department of Pathology, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA.
[Ti] Título:Tumor-Residing Batf3 Dendritic Cells Are Required for Effector T Cell Trafficking and Adoptive T Cell Therapy.
[So] Source:Cancer Cell;31(5):711-723.e4, 2017 May 08.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Effector T cells have the capability of recognizing and killing cancer cells. However, whether tumors can become immune resistant through exclusion of effector T cells from the tumor microenvironment is not known. By using a tumor model resembling non-T cell-inflamed human tumors, we assessed whether adoptive T cell transfer might overcome failed spontaneous priming. Flow cytometric assays combined with intra-vital imaging indicated failed trafficking of effector T cells into tumors. Mechanistically, this was due to the absence of CXCL9/10, which we found to be produced by CD103 dendritic cells (DCs) in T cell-inflamed tumors. Our data indicate that lack of CD103 DCs within the tumor microenvironment dominantly resists the effector phase of an anti-tumor T cell response, contributing to immune escape.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Quimiotaxia de Leucócito
Células Dendríticas/metabolismo
Imunoterapia Adotiva/métodos
Melanoma/terapia
Proteínas Repressoras/metabolismo
Neoplasias Cutâneas/terapia
Linfócitos T/transplante
Evasão Tumoral
[Mh] Termos MeSH secundário: Animais
Antígenos CD/metabolismo
Fatores de Transcrição de Zíper de Leucina Básica/deficiência
Fatores de Transcrição de Zíper de Leucina Básica/genética
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Quimiocina CXCL10/metabolismo
Quimiocina CXCL9/metabolismo
Células Dendríticas/imunologia
Genótipo
Memória Imunológica
Cadeias alfa de Integrinas/metabolismo
Melanoma/imunologia
Melanoma/metabolismo
Melanoma/patologia
Camundongos Knockout
Fenótipo
Proteínas Repressoras/deficiência
Proteínas Repressoras/genética
Transdução de Sinais
Neoplasias Cutâneas/imunologia
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Linfócitos T/imunologia
Linfócitos T/metabolismo
Fatores de Tempo
Carga Tumoral
Microambiente Tumoral
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Basic-Leucine Zipper Transcription Factors); 0 (CTNNB1 protein, mouse); 0 (Chemokine CXCL10); 0 (Chemokine CXCL9); 0 (Cxcl10 protein, mouse); 0 (Cxcl9 protein, mouse); 0 (Integrin alpha Chains); 0 (Repressor Proteins); 0 (SNFT protein, human); 0 (SNFT protein, mouse); 0 (alpha E integrins); 0 (beta Catenin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE


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[PMID]:28432083
[Au] Autor:Shinde P; Liu W; Ménoret A; Luster AD; Vella AT
[Ad] Endereço:Department of Immunology, School of Medicine, University of Connecticut Health, Farmington, Connecticut, USA.
[Ti] Título:Optimal CD4 T cell priming after LPS-based adjuvanticity with CD134 costimulation relies on CXCL9 production.
[So] Source:J Leukoc Biol;102(1):57-69, 2017 Jul.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:LPS is a powerful adjuvant, and although LPS-mediated TLR4 signaling has been exquisitely delineated, the in vivo mechanism of how TLR4 responses impact T cell priming is far less clear. Besides costimulation, TNF and type 1 IFN are dominant cytokines released after TLR4 activation and can shape T cell responses, but other downstream factors have not been examined extensively. Depending on context, we show that IFNαR1 blockade resulted in minor to major effects on specific CD4 T cell clonal expansion. To help explain these differences, it was hypothesized that IFNαR1 blockade would inhibit specific T cell migration by reducing chemokine receptor signaling, but specific CD4 T cells from IFNαR1-blocked mice were readily able to migrate in response to specific chemokines. Next, we examined downstream factors and found that type 1 IFN signaling was necessary for chemokine production, even when mice were immunized with specific Ag with LPS and CD134 costimulation. IFNαR1 signaling promoted CXCL9 and CXCL10 synthesis, suggesting that these chemokines might be involved in the LPS and CD134 costimulation response. After immunization, we show that CXCL9 blockade inhibited CD4 T cell accumulation in the liver but also in LNs, even in the presence of elevated serum IFN-ß levels. Thus, whereas type 1 IFN might have direct effects on primed CD4 T cells, the downstream chemokines that play a role during migration also impact accumulation. In sum, CXCL9 production is a key benchmark for productive CD4 T cell vaccination strategies.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Proliferação Celular/efeitos dos fármacos
Quimiocina CXCL9/imunologia
Lipopolissacarídeos/farmacologia
Receptores OX40/imunologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Quimiocina CXCL10/genética
Quimiocina CXCL10/imunologia
Quimiocina CXCL9/genética
Interferon beta/genética
Interferon beta/imunologia
Camundongos
Camundongos Knockout
Receptor de Interferon alfa e beta/genética
Receptor de Interferon alfa e beta/imunologia
Receptores OX40/genética
Transdução de Sinais/genética
Transdução de Sinais/imunologia
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CXCL10); 0 (Chemokine CXCL9); 0 (Cxcl10 protein, mouse); 0 (Cxcl9 protein, mouse); 0 (Ifnar1 protein, mouse); 0 (Lipopolysaccharides); 0 (Receptors, OX40); 0 (Tlr4 protein, mouse); 0 (Tnfrsf4 protein, mouse); 0 (Toll-Like Receptor 4); 156986-95-7 (Receptor, Interferon alpha-beta); 77238-31-4 (Interferon-beta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171014
[Lr] Data última revisão:
171014
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.1A0616-261RR


  10 / 834 MEDLINE  
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Fotocópia
[PMID]:28387899
[Au] Autor:Lu Y; Lin LY; Tan JG; Deng HP; Li XH; Zhang Z; Li Y; Zhou Z; Xu X; Xie X; Mei SJ
[Ad] Endereço:Infectious Disease Prevention and Control Department, Shenzhen Center for Disease Control and Prevention, Shenzhen, China. yanlu202@163.com.
[Ti] Título:A correlation study between gene polymorphism of Th cell expressed chemokine receptor CXCR3 and its ligand levels with HCV infection prognosis.
[So] Source:Eur Rev Med Pharmacol Sci;21(6):1290-1295, 2017 Mar.
[Is] ISSN:2284-0729
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Chemokine receptor and its ligand participate in viral immunity and HCV infection, which are important inflammatory mediators. The current study showed the different roles of Th cell secreted chemokines CXCR3, CCR5 and CCR6 in chronic liver inflammation after HCV infection. As one important chemokine receptor, the role of polypeptide property and ligand level in HCV prognosis is still unclear. This study aims to investigate gene polymorphism of chemokine genes and ligand level, and their correlation with patient liver function, to provide evidence for HCV prognosis and chronic transition mechanism. PATIENTS AND METHODS: Whole blood samples were collected. Participants were divided into chronic hepatitis, HCV cirrhosis and self-clearance groups. Chemokine level, gene polymorphism of CXCR3 gene at loci rs2280964 and liver index were measured to analyze their correlation with HCV infection or prognosis. RESULTS: Gene polymorphism of CXCR3 at loci rs22809064 is one factor-affecting prognosis of HCV patients. CG genotype at these loci is one independent risk factor affecting chronic HCV infection. IP-10, Mig and I-TAC levels were significantly elevated in chronic hepatitis group or HCV cirrhosis group (p< 0.05 compared to self-clearance group). CONCLUSIONS: Gene polymorphism at rs2280964 locus of chemokine receptor CXCR3 is one possible reason explaining differential processes of chronic transition. CXCR3 ligands IP-10, Mig and I-TAC levels were all significantly elevated in chronic hepatitis and HCV cirrhosis patients, possibly functioning as one clinical index for HCV prognosis.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/metabolismo
Hepatite C Crônica/genética
Receptores CXCR3/genética
[Mh] Termos MeSH secundário: Adulto
Quimiocina CXCL10/sangue
Quimiocina CXCL11/sangue
Quimiocina CXCL9/sangue
Feminino
Hepatite C Crônica/diagnóstico
Seres Humanos
Masculino
Meia-Idade
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CXCL10 protein, human); 0 (CXCL11 protein, human); 0 (CXCL9 protein, human); 0 (CXCR3 protein, human); 0 (Chemokine CXCL10); 0 (Chemokine CXCL11); 0 (Chemokine CXCL9); 0 (Receptors, CXCR3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE



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