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[PMID]:27737517
[Au] Autor:Balada E; Felip L; Ordi-Ros J; Vilardell-Tarrés M
[Ad] Endereço:Research Unit in Systemic Autoimmune Diseases, Vall d'Hebron Research Institute, Universitat Autònoma de Barcelona, Barcelona, Spain.
[Ti] Título:DUSP23 is over-expressed and linked to the expression of DNMTs in CD4 T cells from systemic lupus erythematosus patients.
[So] Source:Clin Exp Immunol;187(2):242-250, 2017 Feb.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We evaluated the transcriptional expression of dual-specificity protein phosphatase 23 (DUSP23) in CD4 T cells from 30 systemic lupus erythematosus (SLE) patients and 30 healthy controls. DUSP23 mRNA levels were considerably higher in the patient group: 1490 ± 1713 versus 294·1 ± 204·2. No association was found between DUSP23 mRNA expression and the presence of typical serological and clinical parameters associated with SLE. Meaningful statistical values were obtained in the patient group between the levels of DUSP23 and integrin subunit alpha L (ITGAL), perforin 1 (PRF1) and CD40L. Similarly, transcript levels of different DNA methylation-related enzymes [DNA methylation-related enzymes (DNMT1, DNMT3A, DNMT3B, MBD2, and MBD4)] were also correlated positively with the expression of DUSP23. In an attempt to counteract the hypomethylation status of the promoters of certain genes known to be over-expressed in SLE, it is possible that DUSP23 acts as a negative regulatory mechanism which ultimately silences the transcription of these epigenetically regulated genes by triggering an increase in the expression of different DNMTs.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Fosfatases de Especificidade Dupla/metabolismo
Lúpus Eritematoso Sistêmico/genética
[Mh] Termos MeSH secundário: Adulto
Antígeno CD11a/metabolismo
Ligante de CD40/metabolismo
Células Cultivadas
Metilação de DNA
Metilases de Modificação do DNA/genética
Metilases de Modificação do DNA/metabolismo
Fosfatases de Especificidade Dupla/genética
Feminino
Seres Humanos
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Meia-Idade
Perforina/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11a Antigen); 126465-35-8 (Perforin); 147205-72-9 (CD40 Ligand); EC 2.1.1.- (DNA Modification Methylases); EC 3.1.3.48 (DUSP23 protein, human); EC 3.1.3.48 (Dual-Specificity Phosphatases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12883


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[PMID]:27539881
[Au] Autor:Kjaergaard AG; Dige A; Nielsen JS; Tønnesen E; Krog J
[Ad] Endereço:Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Aarhus, Denmark. ajk@dadlnet.dk.
[Ti] Título:The use of the soluble adhesion molecules sE-selectin, sICAM-1, sVCAM-1, sPECAM-1 and their ligands CD11a and CD49d as diagnostic and prognostic biomarkers in septic and critically ill non-septic ICU patients.
[So] Source:APMIS;124(10):846-55, 2016 Oct.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Endothelial activation is pivotal in the development and escalation of sepsis. Central to endothelial activation is the endothelial up-regulation of cellular adhesion molecules (CAMs) including E-selectin, ICAM-1, VCAM-1, and PECAM-1. Shed CAMs are also found in circulating soluble forms (sCAMs). We investigated whether sCAMs can be used as biomarkers for the differentiation between septic and non-septic patients. Furthermore, we investigated lymphocyte and monocyte expression of LFA-1 (CD11a/CD18) and VLA-4 (CD49d/CD29) ligands for ICAM-1 and VCAM-1, respectively. Twenty-one septic and 15 critically ill non-septic patients were included. All patients had an APACHE II score above 13 at ICU admission. Fifteen healthy volunteers served as controls. Flow cytometry was used to estimate levels of sE-selectin, sICAM-1, sVCAM-1, sPECAM-1, and the cellular expression of CD11a and CD49d. Levels of sE-selectin, sICAM-1 and sPECAM-1 were higher in the septic patients compared with the non-septic patients and controls at admission and during the observation period. Lymphocyte and monocyte expression of CD11a and CD49d was suppressed or unaltered in the septic patients compared with the non-septic patients and controls. Levels of sE-selectin, sICAM-1, and sPECAM-1 were able to discriminate between septic and non-septic patients, indicating that sCAMs may be potential diagnostic biomarkers of sepsis.
[Mh] Termos MeSH primário: Biomarcadores/análise
Biomarcadores/sangue
Antígeno CD11a/análise
Moléculas de Adesão Celular/sangue
Integrina alfa4/análise
Monócitos/química
Sepse/diagnóstico
[Mh] Termos MeSH secundário: APACHE
Idoso
Estado Terminal
Feminino
Citometria de Fluxo
Seres Humanos
Unidades de Terapia Intensiva
Masculino
Meia-Idade
Prognóstico
Estudos Prospectivos
Sepse/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD11a Antigen); 0 (Cell Adhesion Molecules); 143198-26-9 (Integrin alpha4)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160820
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12585


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[PMID]:27456481
[Au] Autor:Jensen CT; Lang S; Somasundaram R; Soneji S; Sigvardsson M
[Ad] Endereço:Department of Molecular Hematology, Lund University, 22184 Lund, Sweden; and.
[Ti] Título:Identification of Stage-Specific Surface Markers in Early B Cell Development Provides Novel Tools for Identification of Progenitor Populations.
[So] Source:J Immunol;197(5):1937-44, 2016 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Whereas the characterization of B lymphoid progenitors has been facilitated by the identification of lineage- and stage-specific surface markers, the continued identification of differentially expressed proteins increases our capacity to explore normal and malignant B cell development. To identify novel surface markers with stage-specific expression patterns, we explored the reactivity of CD19(+) B cell progenitor cells to Abs targeted to 176 surface proteins. Markers with stage-specific expression were identified using a transgenic reporter gene system subdividing the B cell progenitors into four surface IgM(-) stages. This approach affirmed the utility of known stage-specific markers, as well as identifying additional proteins that selectively marked defined stages of B cell development. Among the stage-specific markers were the cell adhesion proteins CD49E, CD11A, and CD54 that are highly expressed selectively on the most immature progenitors. This work identifies a set of novel stage-specific surface markers that can be used as a complement to the classical staining protocols to explore B lymphocyte development.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Células Precursoras de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD19/análise
Células da Medula Óssea/imunologia
Antígeno CD11a/genética
Antígeno CD11a/imunologia
Moléculas de Adesão Celular/imunologia
Diferenciação Celular
Imunoglobulina M/deficiência
Imunoglobulina M/genética
Integrina alfa5/genética
Integrina alfa5/imunologia
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/imunologia
Ativação Linfocitária
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (CD11a Antigen); 0 (Cell Adhesion Molecules); 0 (Immunoglobulin M); 0 (Integrin alpha5); 126547-89-5 (Intercellular Adhesion Molecule-1)
[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:160727
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600297


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[PMID]:27309860
[Au] Autor:Park YJ; Park MJ; Park S; Lee ES
[Ad] Endereço:Department of Dermatology, Ajou University School of Medicine, Suwon, South Korea.
[Ti] Título:CD11c is upregulated in CD8+ T cells of patients with Behçet's disease.
[So] Source:Clin Exp Rheumatol;34(6 Suppl 102):S86-S91, 2016 Sep-Oct.
[Is] ISSN:0392-856X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Single nucleotide polymorphisms of CD11a and CD11c have been suggested as susceptibility loci in Korean patients with Behçet's disease (BD). As immunoregulatory roles of CD11c+CD8+T cells were previously observed in multiple autoimmune and autoinflammatory diseases, we aimed to investigate CD11a and CD11c in CD4+ and CD8+ subpopulation of BD patients. METHODS: Peripheral-blood mononuclear cells were isolated from 21 patients with active BD, 26 patients with inactive BD, 20 patients with recurrent aphthous ulcers (RAU), and 23 healthy controls (HCs). The surface expression of CD11a and CD11c in CD4+ and CD8+ cell populations was analyzed by flow cytometry, and CD11a and CD11c mRNA and protein levels from puri ed CD8(+) T cells were analyzed using real-time polymerase chain reaction and western blot. RESULTS: The frequencies of CD11a+ and CD11c+ cells were significantly increased in the CD4+ and CD8+ cell populations of active-BD patients, respectively, than that in the HCs. Additionally, both CD11a and CD11c mRNA and protein levels were significantly elevated in the CD8+ T cells of active-BD patients than that in the HCs. CONCLUSIONS: The CD8+ T cells of BD patients exhibited increased CD11c expression levels. Upregulation of CD11c in CD8+ cells may contribute to BD pathogenesis.
[Mh] Termos MeSH primário: Síndrome de Behçet/imunologia
Antígeno CD11c/sangue
Linfócitos T CD8-Positivos/imunologia
[Mh] Termos MeSH secundário: Adulto
Síndrome de Behçet/sangue
Síndrome de Behçet/diagnóstico
Síndrome de Behçet/genética
Biomarcadores/sangue
Western Blotting
Antígeno CD11a/sangue
Antígeno CD11c/genética
Contagem de Linfócito CD4
Linfócitos T CD4-Positivos/imunologia
Estudos de Casos e Controles
Progressão da Doença
Feminino
Citometria de Fluxo
Seres Humanos
Masculino
Meia-Idade
Fenótipo
RNA Mensageiro/sangue
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Indução de Remissão
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD11a Antigen); 0 (CD11c Antigen); 0 (RNA, Messenger)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE


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[PMID]:27283392
[Au] Autor:Guo Y; Zhao M; Lu Q
[Ad] Endereço:Department of Dermatology and Epigenetic Research Center, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
[Ti] Título:Transcription factor RFX1 is ubiquitinated by E3 ligase STUB1 in systemic lupus erythematosus.
[So] Source:Clin Immunol;169:1-7, 2016 08.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic lupus erythematosus (SLE) is a chronic autoimmune disease caused by complex interactions between genes and the environment. The expression level of transcription factor regulatory factor X 1 (RFX1) is reduced in T cells from SLE patients. RFX1 can regulate epigenetic modifications of CD70 and CD11a and plays an important role in the development of SLE. However, the mechanisms that mediate reduction of RFX1 in SLE are unclear. Here, we demonstrate that RFX1 protein expression can be tightly regulated by polyubiquitination-mediated proteosomal degradation via STIP1 homology and U-box containing protein 1 (STUB1). The E3 ligase STUB1 is upregulated in CD4(+)T cells of SLE patients compared to healthy subjects. Overexpression of STUB1 in CD4(+)T cells leads to upregulation of levels of CD70 and CD11a in T cells. The modulation of STUB1 activity may provide a novel therapeutic approach for SLE.
[Mh] Termos MeSH primário: Lúpus Eritematoso Sistêmico/metabolismo
Fator Regulador X1/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
Ubiquitinação
[Mh] Termos MeSH secundário: Adulto
Antígeno CD11a/genética
Antígeno CD11a/metabolismo
Ligante CD27/genética
Ligante CD27/metabolismo
Linfócitos T CD4-Positivos/metabolismo
Células Cultivadas
Feminino
Expressão Gênica
Células HEK293
Seres Humanos
Immunoblotting
Lúpus Eritematoso Sistêmico/genética
Lúpus Eritematoso Sistêmico/imunologia
Masculino
Complexo de Endopeptidases do Proteassoma/metabolismo
Interferência de RNA
Fator Regulador X1/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ubiquitina/metabolismo
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD11a Antigen); 0 (CD27 Ligand); 0 (RFX1 protein, human); 0 (Regulatory Factor X1); 0 (Ubiquitin); EC 2.3.2.27 (STUB1 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160611
[St] Status:MEDLINE


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[PMID]:27107077
[Au] Autor:El-Battrawy I; Tülümen E; Lang S; Akin I; Behnes M; Zhou X; Mavany M; Bugert P; Bieback K; Borggrefe M; Elmas E
[Ad] Endereço:Division of Experimental Cardiology, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany First Department of Medicine, Medical Faculty Mannheim, University Heidelberg, Mannheim, Germany German Center for Cardiovascular Research, Partner Site, Heidelberg-Mannheim, Mannheim, Germany Ibr
[Ti] Título:Expression of Inflammation-related Intercellular Adhesion Molecules in Cardiomyocytes In Vitro and Modulation by Pro-inflammatory Agents.
[So] Source:In Vivo;30(3):213-7, 2016 May-Jun.
[Is] ISSN:1791-7549
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cell-surface adhesion molecules regulate multiple intercellular and intracellular processes and play important roles in inflammation by facilitating leukocyte endothelial transmigration. Whether cardiomyocytes express surface-adhesion molecules related to inflammation and the effect of pro-inflammatory mediators remain unknown. MATERIALS AND METHODS: In the present study, the expression of different cell-adhesion molecules (CD11a, CD11b, CD31, CD62P, CD162, F11 receptor and mucosal vascular addressin cell adhesion molecule 1 (MADCAM1)) and the effect of pro-inflammatory mediators were investigated in an in vitro model of human cardiomyocytes. Cells were supplied as a primary culture of cardiac alpha actin-positive cells from human heart tissue. The cells were incubated for 24 h with 1 U/ml thrombin or 700 ng/ml lipopolysaccharide (LPS) or with a combination of both. The expression of the cell adhesion molecules was measured by flow cytometry. RESULTS: In cultured human cardiomyocytes, 22.8% of cells expressed CD31, 7.1% MADCAM1 and 2.6% F11R. CD11a, CD11b, CD62P and CD162 were expressed by fewer than 2% of the cells at baseline. CD31 expression increased on incubation of cardiomyocytes with thrombin by 26% (p<0.05) and with LPS by 26% (p=0.06). The combination of thrombin and LPS did not result in increased levels of CD31 (p>0.10). The pro-inflammatory agents LPS and thrombin had no effect on the expression of MADCAM1 and F11R. CONCLUSION: Inflammation-related cell-adhesion molecules CD31, MADCAM1 and F11R were shown to be expressed on the surface of human cardiomyocytes in an in vitro model. Incubation with LPS or thrombin resulted in increased expression of CD31, however, it did not modify the expression of the cell adhesion molecules MADCAM1 and F11R.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo
Lipopolissacarídeos/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Trombina/farmacologia
[Mh] Termos MeSH secundário: Actinas/metabolismo
Adulto
Antígeno CD11a/metabolismo
Antígeno CD11b/metabolismo
Células Cultivadas
Citometria de Fluxo
Seres Humanos
Imunoglobulinas/metabolismo
Inflamação/metabolismo
Molécula A de Adesão Juncional/metabolismo
Glicoproteínas de Membrana/metabolismo
Mucoproteínas/metabolismo
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Selectina-P/metabolismo
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (CD11a Antigen); 0 (CD11b Antigen); 0 (Cell Adhesion Molecules); 0 (Immunoglobulins); 0 (Junctional Adhesion Molecule A); 0 (Lipopolysaccharides); 0 (MADCAM1 protein, human); 0 (Membrane Glycoproteins); 0 (Mucoproteins); 0 (P-Selectin); 0 (P-selectin ligand protein); 0 (Platelet Endothelial Cell Adhesion Molecule-1); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160424
[St] Status:MEDLINE


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[PMID]:26994221
[Au] Autor:Askew D; Su CA; Barkauskas DS; Dorand RD; Myers J; Liou R; Nthale J; Huang AY
[Ad] Endereço:Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH 44106; dxa25@case.edu alex.y.huang@case.edu.
[Ti] Título:Transient Surface CCR5 Expression by Naive CD8+ T Cells within Inflamed Lymph Nodes Is Dependent on High Endothelial Venule Interaction and Augments Th Cell-Dependent Memory Response.
[So] Source:J Immunol;196(9):3653-64, 2016 05 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In inflamed lymph nodes, Ag-specific CD4(+) and CD8(+) T cells encounter Ag-bearing dendritic cells and, together, this complex enhances the release of CCL3 and CCL4, which facilitate additional interaction with naive CD8(+) T cells. Although blocking CCL3 and CCL4 has no effect on primary CD8(+) T cell responses, it dramatically impairs the development of memory CD8(+) T cells upon Ag rechallenge. Despite the absence of detectable surface CCR5 expression on circulating native CD8(+) T cells, these data imply that naive CD8(+) T cells are capable of expressing surface CCR5 prior to cognate Ag-induced TCR signaling in inflamed lymph nodes; however, the molecular mechanisms have not been characterized to date. In this study, we show that CCR5, the receptor for CCL3 and CCL4, can be transiently upregulated on a subset of naive CD8(+) T cells and that this upregulation is dependent on direct contact with the high endothelial venule in inflamed lymph node. Binding of CD62L and CD11a on T cells to their ligands CD34 and CD54 on the high endothelial venule can be enhanced during inflammation. This enhanced binding and subsequent signaling promote the translocation of CCR5 molecules from intracellular vesicles to the surface of the CD8(+) T cell. The upregulation of CCR5 on the surface of the CD8(+) T cells increases the number of contacts with Ag-bearing dendritic cells, which ultimately results in increased CD8(+) T cell response to Ag rechallenge.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Memória Imunológica
Linfonodos/imunologia
Receptores CCR5/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno
Antígenos CD34/imunologia
Antígenos CD34/metabolismo
Antígeno CD11a/imunologia
Antígeno CD11a/metabolismo
Células Dendríticas/imunologia
Inflamação
Molécula 1 de Adesão Intercelular/imunologia
Molécula 1 de Adesão Intercelular/metabolismo
Selectina L/imunologia
Selectina L/metabolismo
Linfonodos/citologia
Linfonodos/patologia
Ativação Linfocitária
Camundongos
Receptores CCR5/genética
Linfócitos T Auxiliares-Indutores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (CCR5 protein, mouse); 0 (CD11a Antigen); 0 (Receptors, CCR5); 126547-89-5 (Intercellular Adhesion Molecule-1); 126880-86-2 (L-Selectin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160320
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1501176


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[PMID]:26796515
[Au] Autor:Wang F; Mao L; Hou H; Wu S; Huang M; Yin B; Huang J; Zhu Q; Pan Y; Sun Z
[Ad] Endereço:Department of Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Road 1095,Wuhan 430030, China.
[Ti] Título:The source of Mycobacterium tuberculosis-specific IFN-γ production in peripheral blood mononuclear cells of TB patients.
[So] Source:Int Immunopharmacol;32:39-45, 2016 Mar.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mycobacterium tuberculosis (Mtb)-specific IFN-γ secretion plays important roles in anti-tuberculosis (TB) immunity. Mtb-specific IFN-γ response can be induced in HIV/TB co-infected patients with a low CD4 lymphocyte count; this suggests that the source of Mtb-specific IFN-γ production is not limited in CD4(+) T lymphocytes. Currently, the major sources of Mtb-specific IFN-γ production and the function and phenotype of Mtb-specific IFN-γ-producing cells still remain unclear. Thirty-nine participants (24 active TB patients, 10 HIV/TB co-infected patients, and 5 healthy volunteers) were recruited according to conventional tests and Mtb-specific IFN-γ ELISPOT assay. Multicolor flow cytometry was used to investigate the production of intracellular IFN-γ in peripheral blood mononuclear cells (PBMCs) after Mtb-specific antigen stimulation. Our results showed that CD4(+), CD8(+) T cells and NK cells are all major sources of Mtb-specific IFN-γ production in PBMCs of TB patients. Moreover, CD8(+) T cells are the highest number of Mtb-specific IFN-γ-producing cells in HIV/TB co-infected patients. Although the activity of NK cells is significantly reduced in TB patients when compared with healthy controls, Mtb-specific antigen stimulation induces a significant increase in NK cell activity. We also showed that CD45RO is the characteristic marker of Mtb-specific IFN-γ-producing T cells but not that of Mtb-specific IFN-γ-producing NK cells in peripheral blood. High expression of CD11a may be the characteristic feature of Mtb-specific IFN-γ-producing NK cells. This study put forward a new insight on the source of antigen-specific IFN-γ-production in PBMCs of TB patients.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Interferon gama/imunologia
Células Matadoras Naturais/imunologia
Mycobacterium tuberculosis/imunologia
Tuberculose Pulmonar/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígeno CD11a/imunologia
Feminino
Infecções por HIV/imunologia
Seres Humanos
Antígenos Comuns de Leucócito/imunologia
Masculino
Meia-Idade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD11a Antigen); 82115-62-6 (Interferon-gamma); EC 3.1.3.48 (Leukocyte Common Antigens)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE


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[PMID]:26518418
[Au] Autor:Sun L; Liu H; Jiang H; Wei M; Liang S; Wang M; Shi K; He Q
[Ad] Endereço:School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
[Ti] Título:Macrophages Are Involved in Gut Bacterial Translocation and Reversed by Lactobacillus in Experimental Uremia.
[So] Source:Dig Dis Sci;61(6):1534-44, 2016 Jun.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Uremia causes gut microbiome dysbiosis, which is characterized by a reduction in beneficial bacteria. Intestinal bacterial translocation (BT) contributes to microinflammation in uremia, which is associated with adverse outcomes. Whether macrophages are involved in BT remains unclear. AIMS: We investigated the involvement of macrophages in BT and microinflammation in uremic rats and whether Lactobacillus LB can influence macrophage activity. METHODS: Male Sprague-Dawley rats were randomly divided into three groups: sham, uremia, and uremia + probiotic. Macrophages and GFP-labeled tracer bacteria in intestinal and extraintestinal tissues were observed by fluorescence microscopy. The macrophage ultrastructure was examined by transmission electron microscopy. Immunochemistry was used to analyze the expression of cluster of differentiation 11a (CD11a), inducible nitric oxide synthase (iNOS), and intercellular adhesion molecule-1 (ICAM-1). RT-PCR and Western blot were employed to assess the mRNA and protein expression of early growth response gene 1 (EGR1) and toll-like receptor 4 (TLR4). RESULTS: In uremic rats, the colocalization of GFP-labeled tracer bacteria and macrophages was visible in intestinal and extraintestinal tissues. Compared with the sham group, the uremic macrophages showed fewer cytoplasmic protrusions and pseudopodia. Administration of Lactobacillus LB restored the protrusions and pseudopodia. Compared with the sham group, the uremia group exhibited macrophages with higher staining intensities for CD11a, iNOS, and ICAM-1, and higher mRNA and protein expression of TLR4 and EGR1. CONCLUSIONS: Intestinal macrophages in the uremic rats are polarized toward a proinflammatory phenotype, resulting in microinflammation. Macrophages with impaired phagocytic function are associated with BT. Lactobacillus LB reduces BT by enhancing macrophage phagocytosis.
[Mh] Termos MeSH primário: Translocação Bacteriana/fisiologia
Trato Gastrointestinal/microbiologia
Lactobacillus/fisiologia
Macrófagos/fisiologia
Uremia/patologia
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Antígeno CD11a/genética
Antígeno CD11a/metabolismo
Proteína 1 de Resposta de Crescimento Precoce/genética
Proteína 1 de Resposta de Crescimento Precoce/metabolismo
Endotoxinas/metabolismo
Regulação da Expressão Gênica/fisiologia
Inflamação/sangue
Inflamação/metabolismo
Molécula 1 de Adesão Intercelular/genética
Molécula 1 de Adesão Intercelular/metabolismo
Mucosa Intestinal/citologia
Mucosa Intestinal/microbiologia
Mucosa Intestinal/patologia
Masculino
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Receptor 4 Toll-Like/genética
Receptor 4 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CD11a Antigen); 0 (Early Growth Response Protein 1); 0 (Egr1 protein, rat); 0 (Endotoxins); 0 (RNA, Messenger); 0 (Tlr4 protein, rat); 0 (Toll-Like Receptor 4); 126547-89-5 (Intercellular Adhesion Molecule-1); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:151101
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-015-3950-z


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[PMID]:26116356
[Au] Autor:Alikhan MA; Summers SA; Gan PY; Chan AJ; Khouri MB; Ooi JD; Ghali JR; Odobasic D; Hickey MJ; Kitching AR; Holdsworth SR
[Ad] Endereço:Centre for Inflammatory Diseases, Department of Medicine, Monash University, Clayton, Victoria, Australia;
[Ti] Título:Endogenous Toll-Like Receptor 9 Regulates AKI by Promoting Regulatory T Cell Recruitment.
[So] Source:J Am Soc Nephrol;27(3):706-14, 2016 Mar.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Toll-like receptor 9 (TLR9) enhances proinflammatory responses, but whether it can act in a regulatory capacity remains to be established. In experimental murine AKI induced by cisplatin, Tlr9(-/-) mice developed enhanced renal injury and exhibited fewer intrarenal regulatory T cells (Tregs) compared with genetically intact mice. A series of reconstitution and depletion studies defined a role for TLR9 in maintaining Treg-mediated homeostasis in cisplatin-induced AKI. When Rag1(-/-) mice were reconstituted with nonregulatory CD25(-) splenocytes from wild-type (WT) or Tlr9(-/-) mice, AKI was similarly enhanced. However, when Rag1(-/-) mice were reconstituted with CD4(+)CD25(+) regulatory cells, WT CD4(+)CD25(+) cells were more renoprotective and localized to the kidney more efficiently than Tlr9(-/-) CD4(+)CD25(+) cells. In Treg-depleted Foxp3(DTR) mice, reconstitution with naive WT CD4(+)CD25(+) cells resulted in less severe AKI than did reconstitution with Tlr9(-/-) Tregs. Tlr9(-/-) mice were not deficient in CD4(+)CD25(+) cells, and WT and TLR9-deficient Tregs had similar suppressive function ex vivo. However, expression of adhesion molecules important in Treg trafficking was reduced on peripheral CD4(+)CD25(+) cells from Tlr9(-/-) mice. In conclusion, we identified a pathway by which TLR9 promotes renal Treg accumulation in AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/imunologia
Lesão Renal Aguda/metabolismo
Ativação Linfocitária
Linfócitos T Reguladores/imunologia
Receptor Toll-Like 9/fisiologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Animais
Antígeno CD11a/metabolismo
Cisplatino
Proteínas de Homeodomínio/genética
Receptores de Hialuronatos/metabolismo
Integrina alfa4/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Linfócitos T Reguladores/metabolismo
Receptor Toll-Like 9/genética
Receptor Toll-Like 9/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD11a Antigen); 0 (Homeodomain Proteins); 0 (Hyaluronan Receptors); 0 (Toll-Like Receptor 9); 128559-51-3 (RAG-1 protein); 143198-26-9 (Integrin alpha4); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150628
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2014090927



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