Database : MEDLINE
Search on : Interleukin-2 and Receptor and beta and Subunit [Words]
References found : 2082 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 209 go to page                         

  1 / 2082 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 29307521
[Au] Autor:Han W; Ni Q; Liu K; Yao Y; Zhao D; Liu X; Chen Y
[Ad] Address:Department of Laboratory Medicine, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, China; Key Laboratory of Clinical In Vitro Diagnostic Techniques of Zhejiang Province, 79 Qingchun Road, Hangzhou 310003, China.
[Ti] Title:Decreased CD122 on CD56 NK associated with its impairment in asymptomatic chronic HBV carriers with high levels of HBV DNA, HBsAg and HBeAg.
[So] Source:Life Sci;195:53-60, 2018 Feb 15.
[Is] ISSN:1879-0631
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:AIMS: NK cells play important roles in inhibiting HBV replication and preventing HBV infection. However, NK-cell dysfunction has not been fully studied in asymptomatic chronic HBV carriers (ASC). This study aims to assess decreased expression of CD122 associated with impaired NK cells and the restoration of NK cells with IL-2 and IL-15 stimulation. MAIN METHODS: The experiments were performed by flow cytometer, cytotoxicity assay, ELISA and western blotting. KEY FINDINGS: The reduced CD122 on CD56 NK cells and CD56 NK cells is associated with high levels of HBV DNA, HBsAg or HBeAg in ASCs, in which CD56 NK-cell impairment is observed. Moreover, decreased IFN-γ and degranulation and low cytotoxicity by CD56 NK cells after CD122 blockade were revealed. IL-2 and/or IL-15 can restore impaired CD56 NK cells, together with increased p-STAT5, which can be reversed by CD122 blockade. Additionally, IL-2 or IL-15 can enhance IFN-α2-activated CD56 NK-cell immune responses via up-regulating interferon alpha and beta receptor subunit 2 (IFNAR2). SIGNIFICANCE: Down-regulated CD122 on CD56 NK cell in ASCs with massive viral antigens and high viremia is associated with its impairment, which can be restored by IL-2 and/or IL-15, or combined with IFN-α2.
[Mh] MeSH terms primary: CD56 Antigen/biosynthesis
DNA, Viral/biosynthesis
Hepatitis B Surface Antigens/blood
Hepatitis B e Antigens/blood
Hepatitis B virus/metabolism
Hepatitis B/metabolism
Interleukin-2 Receptor beta Subunit/biosynthesis
Killer Cells, Natural/metabolism
[Mh] MeSH terms secundary: Adult
CD56 Antigen/genetics
Carrier State
DNA, Viral/genetics
Female
Hepatitis B virus/genetics
Humans
Interferon-gamma/biosynthesis
Interleukin-15/pharmacology
Interleukin-2/pharmacology
Interleukin-2 Receptor beta Subunit/genetics
Male
Receptor, Interferon alpha-beta/biosynthesis
Receptor, Interferon alpha-beta/genetics
STAT5 Transcription Factor/biosynthesis
STAT5 Transcription Factor/genetics
Viremia/blood
Viremia/virology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (CD56 Antigen); 0 (DNA, Viral); 0 (Hepatitis B Surface Antigens); 0 (Hepatitis B e Antigens); 0 (IFNAR2 protein, human); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Interleukin-2 Receptor beta Subunit); 0 (STAT5 Transcription Factor); 156986-95-7 (Receptor, Interferon alpha-beta); 82115-62-6 (Interferon-gamma)
[Em] Entry month:1802
[Cu] Class update date: 180208
[Lr] Last revision date:180208
[Js] Journal subset:IM
[Da] Date of entry for processing:180109
[St] Status:MEDLINE

  2 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28901888
[Au] Autor:Tzang BS; Liu CH; Hsu KC; Chen YH; Huang CY; Hsu TC
[Ad] Address:1Institute of Biochemistry, Microbiology and Immunology,Chung Shan Medical University,Taichung 402,Taiwan,ROC.
[Ti] Title:Effects of oral Lactobacillus administration on antioxidant activities and CD4+CD25+forkhead box P3 (FoxP3)+ T cells in NZB/W F1 mice.
[So] Source:Br J Nutr;118(5):333-342, 2017 Sep.
[Is] ISSN:1475-2662
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterised by a dysregulation of the immune system, which causes inflammation responses, excessive oxidative stress and a reduction in the number of cluster of differentiation (CD)4+CD25+forkhead box P3 (FoxP3)+ T cells. Supplementation with certain Lactobacillus strains has been suggested to be beneficial in the comprehensive treatment of SLE. However, little is known about the effect and mechanism of certain Lactobacillus strains on SLE. To investigate the effects of Lactobacillus on SLE, NZB/W F1 mice were orally gavaged with Lactobacillus paracasei GMNL-32 (GMNL-32), Lactobacillus reuteri GMNL-89 (GMNL-89) and L. reuteri GMNL-263 (GMNL-263). Supplementation with GMNL-32, GMNL-89 and GMNL-263 significantly increased antioxidant activity, reduced IL-6 and TNF-α levels and significantly decreased the toll-like receptors/myeloid differentiation primary response gene 88 signalling in NZB/W F1 mice. Notably, supplementation with GMNL-263, but not GMNL-32 and GMNL-89, in NZB/W F1 mice significantly increased the differentiation of CD4+CD25+FoxP3+ T cells. These findings reveal beneficial effects of GMNL-32, GMNL-89 and GMNL-263 on NZB/W F1 mice and suggest that these specific Lactobacillus strains can be used as part of a comprehensive treatment of SLE patients.
[Mh] MeSH terms primary: Antioxidants/metabolism
CD4-Positive T-Lymphocytes/cytology
Lactobacillus
Probiotics/administration & dosage
[Mh] MeSH terms secundary: Administration, Oral
Animals
CD4-Positive T-Lymphocytes/metabolism
Disease Models, Animal
Female
Forkhead Transcription Factors/metabolism
Glutathione/blood
Interleukin-2 Receptor alpha Subunit/metabolism
Interleukin-6/blood
Lactobacillus/classification
Lupus Erythematosus, Systemic/therapy
Mice
Mice, Inbred NZB
RNA, Messenger/blood
Thiobarbiturates/blood
Toll-Like Receptors/blood
Tumor Necrosis Factor-alpha/blood
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antioxidants); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-6); 0 (RNA, Messenger); 0 (Thiobarbiturates); 0 (Toll-Like Receptors); 0 (Tumor Necrosis Factor-alpha); GAN16C9B8O (Glutathione); M1YZW5SS7C (thiobarbituric acid)
[Em] Entry month:1709
[Cu] Class update date: 170921
[Lr] Last revision date:170921
[Js] Journal subset:IM
[Da] Date of entry for processing:170914
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002112

  3 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28866095
[Au] Autor:Sadras T; Heatley SL; Kok CH; Dang P; Galbraith KM; McClure BJ; Muskovic W; Venn NC; Moore S; Osborn M; Revesz T; Moore AS; Hughes TP; Yeung D; Sutton R; White DL
[Ad] Address:Cancer Theme, South Australian Health & Medical Research Institute, Adelaide, SA, Australia; Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
[Ti] Title:Differential expression of MUC4, GPR110 and IL2RA defines two groups of CRLF2-rearranged acute lymphoblastic leukemia patients with distinct secondary lesions.
[So] Source:Cancer Lett;408:92-101, 2017 Nov 01.
[Is] ISSN:1872-7980
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:CRLF2-rearrangements (CRLF2-r) occur frequently in Ph-like B-ALL, a high-risk ALL sub-type characterized by a signaling profile similar to Ph + ALL, however accumulating evidence indicates genetic heterogeneity within CRLF2-r ALL. We performed thorough genomic characterization of 35 CRLF2-r cases (P2RY8-CRLF2 n = 18; IGH-CRLF2 n = 17). Activating JAK2 mutations were present in 34% of patients, and a CRLF2-F232C mutation was identified in an additional 17%. IKZF1 deletions were detected in 63% of cases. The majority of patients (26/35) classified as Ph-like, and these were characterized by significantly higher levels of MUC4, GPR110 and IL2RA/CD25. In addition, Ph-like CRLF2-r samples were significantly enriched for IKZF1 deletions, JAK2/CRLF2 mutations and increased expression of JAK/STAT target genes (CISH, SOCS1), suggesting that mutation-driven CRLF2/JAK2 activation is more frequent in this sub-group. Less is known about the genomics of CRLF2-r cases lacking JAK2-pathway mutations, but KRAS/NRAS mutations were identified in 4/9 non-Ph-like samples. This work highlights the heterogeneity of secondary lesions which may arise and influence intracellular-pathway activation in CRLF2-r patients, and importantly presents distinct therapeutic targets within a group of patients harboring identical primary translocations, for whom efficient directed therapies are currently lacking.
[Mh] MeSH terms primary: Gene Expression Regulation, Leukemic
Gene Rearrangement
Interleukin-2 Receptor alpha Subunit/metabolism
Mucin-4/metabolism
Oncogene Proteins/metabolism
Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology
Receptors, Cytokine/genetics
Receptors, G-Protein-Coupled/metabolism
[Mh] MeSH terms secundary: Female
Humans
Interleukin-2 Receptor alpha Subunit/genetics
Janus Kinase 2/genetics
Janus Kinase 2/metabolism
Mucin-4/genetics
Mutation/genetics
Oncogene Proteins/genetics
Philadelphia Chromosome
Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism
Prognosis
Receptors, G-Protein-Coupled/genetics
Tumor Cells, Cultured
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (CRLF2 protein, human); 0 (GPR110 protein, human); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (MUC4 protein, human); 0 (Mucin-4); 0 (Oncogene Proteins); 0 (Receptors, Cytokine); 0 (Receptors, G-Protein-Coupled); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)
[Em] Entry month:1711
[Cu] Class update date: 171101
[Lr] Last revision date:171101
[Js] Journal subset:IM
[Da] Date of entry for processing:170904
[St] Status:MEDLINE

  4 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28855314
[Au] Autor:Muschaweckh A; Petermann F; Korn T
[Ad] Address:Klinikum Rechts der Isar, Neurologische Klinik, Technische Universität München, 81675 Munich, Germany; and.
[Ti] Title:IL-1ß and IL-23 Promote Extrathymic Commitment of CD27 CD122 γδ T Cells to γδT17 Cells.
[So] Source:J Immunol;199(8):2668-2679, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:γδT17 cells are a subset of γδ T cells committed to IL-17 production and are characterized by the expression of IL-23R and CCR6 and lack of CD27 expression. γδT17 cells are believed to arise within a narrow time window during prenatal thymic development. In agreement with this concept, we show in this study that adult recipient mice of (IL-23R reporter) bone marrow selectively lack IL-23R γδT17 cells. Despite their absence in secondary lymphoid tissues during homeostasis, γδT17 cells emerge in bone marrow chimeric mice upon induction of skin inflammation by topical treatment with imiquimod cream (Aldara). We demonstrate that IL-1ß and IL-23 together are able to promote the development of bona fide γδT17 cells from peripheral CD122 IL-23R γδ T cells, whereas CD122 γδ T cells fail to convert into γδT17 cells and remain stable IFN-γ producers (γδT1 cells). IL-23 is instrumental in expanding extrathymically generated γδT17 cells. In particular, TCR-Vγ4 chain-expressing CD122 IL-23R γδ T cells are induced to express IL-23R and IL-17 outside the thymus during skin inflammation. In contrast, TCR-Vγ1 γδ T cells largely resist this process because prior TCR engagement in the thymus has initiated their commitment to the γδT1 lineage. In summary, our data reveal that the peripheral pool of γδ T cells retains a considerable degree of plasticity because it harbors "naive" precursors, which can be induced to produce IL-17 and replenish peripheral niches that are usually occupied by thymus-derived γδT17 cells.
[Mh] MeSH terms primary: Interleukin-17/metabolism
Psoriasis/immunology
T-Lymphocytes/physiology
[Mh] MeSH terms secundary: Aminoquinolines
Animals
Cell Differentiation
Cells, Cultured
Disease Models, Animal
Humans
Interleukin-1beta/metabolism
Interleukin-2 Receptor beta Subunit/metabolism
Interleukin-23/metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Receptors, Antigen, T-Cell, gamma-delta/metabolism
Receptors, Interleukin/genetics
Tumor Necrosis Factor Receptor Superfamily, Member 7/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Aminoquinolines); 0 (Interleukin-17); 0 (Interleukin-1beta); 0 (Interleukin-2 Receptor beta Subunit); 0 (Interleukin-23); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-23 receptor, mouse); P1QW714R7M (imiquimod)
[Em] Entry month:1711
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170901
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700287

  5 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28803486
[Au] Autor:Osherov M; Milo R
[Ad] Address:a Department of Neurology, Barzilai University Medical Center, Ashkelon, Faculty of Health Sciences , Ben-Gurion University of the Negev , Ashkelon , Israel.
[Ti] Title:Daclizumab for the treatment of adults with relapsing forms of multiple sclerosis.
[So] Source:Expert Rev Clin Pharmacol;10(10):1037-1047, 2017 Oct.
[Is] ISSN:1751-2441
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The goal of the article is to review the mechanism of action and the use of daclizumab, a humanized monoclonal antibody (mAb) against the alpha subunit of the high affinity interleukin-2 (IL-2) receptor, in the treatment of Multiple Sclerosis (MS). Areas covered: PubMed was searched for the terms 'daclizumab' and 'multiple sclerosis'. The mechanisms of action, pharmacokinetics and pharmacodynamics, major studies, side effects and drug interactions of daclizumab in MS are discussed. Expert commentary: Monthly daclizumab-beta [DAC-beta, formerly daclizumab high yield process (DAC HYP), approved as ZINBRYTA®, which has a different form and structure than an earlier form of daclizumab], is an effective and convenient treatment option for patients with relapsing forms of MS who have failed other treatment, or as a first-line option in highly active MS patients. IL-2 signaling modulation by daclizumab constitutes a novel mechanism of action which may also underlie the adverse and serious adverse events and risk profile of the drug that requires appropriate patient selection, monitoring and risk-mitigation programs.
[Mh] MeSH terms primary: Antibodies, Monoclonal, Humanized/therapeutic use
Immunoglobulin G/therapeutic use
Immunosuppressive Agents/therapeutic use
Multiple Sclerosis, Relapsing-Remitting/drug therapy
[Mh] MeSH terms secundary: Adult
Animals
Antibodies, Monoclonal, Humanized/adverse effects
Antibodies, Monoclonal, Humanized/pharmacology
Drug Interactions
Humans
Immunoglobulin G/adverse effects
Immunoglobulin G/pharmacology
Immunosuppressive Agents/adverse effects
Immunosuppressive Agents/pharmacology
Interleukin-2 Receptor alpha Subunit/antagonists & inhibitors
Interleukin-2 Receptor alpha Subunit/immunology
Multiple Sclerosis, Relapsing-Remitting/immunology
Patient Selection
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antibodies, Monoclonal, Humanized); 0 (Immunoglobulin G); 0 (Immunosuppressive Agents); 0 (Interleukin-2 Receptor alpha Subunit); CUJ2MVI71Y (daclizumab)
[Em] Entry month:1710
[Cu] Class update date: 171013
[Lr] Last revision date:171013
[Js] Journal subset:IM
[Da] Date of entry for processing:170815
[St] Status:MEDLINE
[do] DOI:10.1080/17512433.2017.1366854

  6 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28724578
[Au] Autor:Miyagawa I; Nakayamada S; Nakano K; Yamagata K; Sakata K; Yamaoka K; Tanaka Y
[Ad] Address:First Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
[Ti] Title:Induction of Regulatory T Cells and Its Regulation with Insulin-like Growth Factor/Insulin-like Growth Factor Binding Protein-4 by Human Mesenchymal Stem Cells.
[So] Source:J Immunol;199(5):1616-1625, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Human mesenchymal stem cells (MSCs) are multipotent and exert anti-inflammatory effects, but the underlying mechanism remains to be elucidated. In the current study, we investigated the regulatory mechanism of regulatory T cell (Treg) induction through the growth factors released by human MSCs. Human naive CD4 T cells were stimulated with anti-CD3/28 Abs and cocultured with human MSC culture supernatant for 48 h. The proliferation and cytokine production of CD4 T cells and surface molecule expression on CD4 T cells were evaluated. The proliferation of anti-CD3/28 Abs-stimulated CD4 T cells was suppressed by the addition of human MSC culture supernatant; in addition, the production of IL-10 and IL-4 increased. The human MSC culture supernatant induced CD4 FOXP3 Tregs that expressed CD25, CTLA-4, glucocorticoid-induced TNFR-related protein, insulin-like growth factor (IGF)-1R, and IGF-2R, showing antiproliferative activity against CD4 T cells. In addition, the induction of Tregs by human MSC culture supernatant was enhanced by the addition of IGF and suppressed by the inhibition of IGF-1R. In contrast, a significant amount of IGF binding protein (IGFBP)-4, an inhibitor of IGF action, was detected in the human MSC culture supernatant. After neutralization of IGFBP-4 in the human MSC culture supernatant by anti-IGFBP-4 Ab, Treg numbers increased significantly. Thus, our results raise the possibility that human MSC actions also involve a negative-regulatory mechanism that suppresses Treg proliferation by releasing IGFBP-4. The results of this study suggest that regulation of IGF may be important for treatments using human MSCs.
[Mh] MeSH terms primary: Immune Tolerance
Insulin-Like Growth Factor Binding Protein 4/metabolism
Mesenchymal Stromal Cells/physiology
Somatomedins/metabolism
T-Lymphocytes, Regulatory/immunology
[Mh] MeSH terms secundary: Antibodies, Neutralizing/pharmacology
CTLA-4 Antigen/metabolism
Cell Proliferation
Cells, Cultured
Coculture Techniques
Forkhead Transcription Factors/metabolism
Glucocorticoid-Induced TNFR-Related Protein/metabolism
Humans
Insulin-Like Growth Factor Binding Protein 4/immunology
Interleukin-2 Receptor alpha Subunit/metabolism
Receptor, IGF Type 1/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antibodies, Neutralizing); 0 (CTLA-4 Antigen); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Glucocorticoid-Induced TNFR-Related Protein); 0 (Insulin-Like Growth Factor Binding Protein 4); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Somatomedins); EC 2.7.10.1 (Receptor, IGF Type 1)
[Em] Entry month:1709
[Cu] Class update date: 170929
[Lr] Last revision date:170929
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170721
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600230

  7 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28716979
[Au] Autor:Bustamante A; López-Cancio E; Pich S; Penalba A; Giralt D; García-Berrocoso T; Ferrer-Costa C; Gasull T; Hernández-Pérez M; Millan M; Rubiera M; Cardona P; Cano L; Quesada H; Terceño M; Silva Y; Castellanos M; Garces M; Reverté S; Ustrell X; Marés R; Baiges JJ; Serena J; Rubio F; Salas E; Dávalos A; Montaner J
[Ad] Address:From the Neurovascular Research Laboratory, Vall d'Hebron Institut de Recerca (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain (A.B., A.P., D.G., T.G.-B., J.M.); Stroke Unit, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain (E.L.-C., M.H.-P., M.M., A
[Ti] Title:Blood Biomarkers for the Early Diagnosis of Stroke: The Stroke-Chip Study.
[So] Source:Stroke;48(9):2419-2425, 2017 Sep.
[Is] ISSN:1524-4628
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Stroke diagnosis could be challenging in the acute phase. We aimed to develop a blood-based diagnostic tool to differentiate between real strokes and stroke mimics and between ischemic and hemorrhagic strokes in the hyperacute phase. METHODS: The Stroke-Chip was a prospective, observational, multicenter study, conducted at 6 Stroke Centers in Catalonia. Consecutive patients with suspected stroke were enrolled within the first 6 hours after symptom onset, and blood samples were drawn immediately after admission. A 21-biomarker panel selected among previous results and from the literature was measured by immunoassays. Outcomes were differentiation between real strokes and stroke mimics and between ischemic and hemorrhagic strokes. Predictive models were developed by combining biomarkers and clinical variables in logistic regression models. Accuracy was evaluated with receiver operating characteristic curves. RESULTS: From August 2012 to December 2013, 1308 patients were included (71.9% ischemic, 14.8% stroke mimics, and 13.3% hemorrhagic). For stroke versus stroke mimics comparison, no biomarker resulted included in the logistic regression model, but it was only integrated by clinical variables, with a predictive accuracy of 80.8%. For ischemic versus hemorrhagic strokes comparison, NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) >4.9 (odds ratio, 2.40; 95% confidence interval, 1.55-3.71; <0.0001) and endostatin >4.7 (odds ratio, 2.02; 95% confidence interval, 1.19-3.45; =0.010), together with age, sex, blood pressure, stroke severity, atrial fibrillation, and hypertension, were included in the model. Predictive accuracy was 80.6%. CONCLUSIONS: The studied biomarkers were not sufficient for an accurate differential diagnosis of stroke in the hyperacute setting. Additional discovery of new biomarkers and improvement on laboratory techniques seem necessary for achieving a molecular diagnosis of stroke.
[Mh] MeSH terms primary: Brain Ischemia/blood
Cerebral Hemorrhage/blood
Stroke/blood
[Mh] MeSH terms secundary: Aged
Aged, 80 and over
Amine Oxidase (Copper-Containing)/blood
Apolipoprotein C-III/blood
Biomarkers/blood
Brain Ischemia/diagnosis
Case-Control Studies
Caspase 3/blood
Cell Adhesion Molecules/blood
Cerebral Hemorrhage/diagnosis
Chemokine CXCL1/blood
Endostatins/blood
Fas Ligand Protein/blood
Female
Fibrin Fibrinogen Degradation Products/metabolism
Fibronectins/blood
HSC70 Heat-Shock Proteins/blood
Humans
Insulin-Like Growth Factor Binding Protein 3/blood
Interleukin Receptor Common gamma Subunit/blood
Interleukin-17/blood
Interleukin-6/blood
Logistic Models
Male
Matrix Metalloproteinase 9/blood
Middle Aged
Natriuretic Peptide, Brain/blood
Nerve Growth Factor/blood
Neural Cell Adhesion Molecules/blood
Odds Ratio
Peptide Fragments/blood
Phosphopyruvate Hydratase/blood
Prospective Studies
ROC Curve
Receptors, Tumor Necrosis Factor, Type I/blood
S100 Calcium Binding Protein beta Subunit/blood
Stroke/diagnosis
von Willebrand Factor/metabolism
[Pt] Publication type:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Name of substance:0 (Apolipoprotein C-III); 0 (Biomarkers); 0 (Cell Adhesion Molecules); 0 (Chemokine CXCL1); 0 (Endostatins); 0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (Fibrin Fibrinogen Degradation Products); 0 (Fibronectins); 0 (HSC70 Heat-Shock Proteins); 0 (HSPA8 protein, human); 0 (IGFBP3 protein, human); 0 (IL17A protein, human); 0 (IL2RG protein, human); 0 (IL6 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-17); 0 (Interleukin-6); 0 (NGF protein, human); 0 (Neural Cell Adhesion Molecules); 0 (Peptide Fragments); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100B protein, human); 0 (fibrin fragment D); 0 (pro-brain natriuretic peptide (1-76)); 0 (von Willebrand Factor); 114471-18-0 (Natriuretic Peptide, Brain); 9061-61-4 (Nerve Growth Factor); EC 1.4.3.21 (AOC3 protein, human); EC 1.4.3.21 (Amine Oxidase (Copper-Containing)); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Entry month:1709
[Cu] Class update date: 170926
[Lr] Last revision date:170926
[Js] Journal subset:IM
[Da] Date of entry for processing:170719
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017076

  8 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28710254
[Au] Autor:Bhela S; Varanasi SK; Jaggi U; Sloan SS; Rajasagi NK; Rouse BT
[Ad] Address:Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996.
[Ti] Title:The Plasticity and Stability of Regulatory T Cells during Viral-Induced Inflammatory Lesions.
[So] Source:J Immunol;199(4):1342-1352, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Ocular infection with HSV causes a chronic T cell-mediated inflammatory lesion in the cornea. Lesion severity is affected by the balance of different CD4 T cell subsets, with greater severity occurring when the activity of regulatory T cells (Tregs) is compromised. In this study, fate-mapping mice were used to assess the stability of Treg function in ocular lesions. We show that cells that were once Foxp3 functional Tregs may lose Foxp3 and become Th1 cells that could contribute to lesion expression. The instability primarily occurred with IL-2R Tregs and was shown, in part, to be the consequence of exposure to IL-12. Lastly, in vitro-generated induced Tregs (iTregs) were shown to be highly plastic and capable of inducing stromal keratitis when adoptively transferred into Rag1 mice, with 95% of iTregs converting into ex-Tregs in the cornea. This plasticity of iTregs could be prevented when they were generated in the presence of vitamin C and retinoic acid. Importantly, adoptive transfer of these stabilized iTregs to HSV-1-infected mice prevented the development of stromal keratitis lesions more effectively than did control iTregs. Our results demonstrate that CD25 Treg and iTreg instability occurs during a viral immunoinflammatory lesion and that its control may help to avoid lesion chronicity.
[Mh] MeSH terms primary: Cell Plasticity
Cornea/immunology
Cornea/pathology
Herpesvirus 1, Human/immunology
Keratitis, Herpetic/immunology
T-Lymphocytes, Regulatory/immunology
Th1 Cells/immunology
[Mh] MeSH terms secundary: Adoptive Transfer
Animals
Ascorbic Acid/pharmacology
CD4-Positive T-Lymphocytes/immunology
Cell Differentiation
Cornea/virology
Female
Forkhead Transcription Factors/analysis
Homeodomain Proteins/genetics
Interleukin-12/immunology
Interleukin-12/metabolism
Interleukin-2 Receptor alpha Subunit/genetics
Interleukin-2 Receptor alpha Subunit/immunology
Keratitis, Herpetic/physiopathology
Keratitis, Herpetic/virology
Lymphocyte Activation
Mice
T-Lymphocyte Subsets/immunology
T-Lymphocyte Subsets/physiology
T-Lymphocytes, Regulatory/drug effects
T-Lymphocytes, Regulatory/physiology
Th1 Cells/physiology
Tretinoin/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Homeodomain Proteins); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 128559-51-3 (RAG-1 protein); 187348-17-0 (Interleukin-12); 5688UTC01R (Tretinoin); PQ6CK8PD0R (Ascorbic Acid)
[Em] Entry month:1710
[Cu] Class update date: 171016
[Lr] Last revision date:171016
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170716
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700520

  9 / 2082 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 28678791
[Au] Autor:Charych D; Khalili S; Dixit V; Kirk P; Chang T; Langowski J; Rubas W; Doberstein SK; Eldon M; Hoch U; Zalevsky J
[Ad] Address:Nektar Therapeutics, San Francisco, California, United States of America.
[Ti] Title:Modeling the receptor pharmacology, pharmacokinetics, and pharmacodynamics of NKTR-214, a kinetically-controlled interleukin-2 (IL2) receptor agonist for cancer immunotherapy.
[So] Source:PLoS One;12(7):e0179431, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cytokines are potent immune modulating agents but are not ideal medicines in their natural form due to their short half-life and pleiotropic systemic effects. NKTR-214 is a clinical-stage biologic that comprises interleukin-2 (IL2) protein bound by multiple releasable polyethylene glycol (PEG) chains. In this highly PEG-bound form, the IL2 is inactive; therefore, NKTR-214 is a biologic prodrug. When administered in vivo, the PEG chains slowly release, creating a cascade of increasingly active IL2 protein conjugates bound by fewer PEG chains. The 1-PEG-IL2 and 2-PEG-IL2 species derived from NKTR-214 are the most active conjugated-IL2 species. Free-IL2 protein is undetectable in vivo as it is eliminated faster than formed. The PEG chains on NKTR-214 are located at the region of IL2 that contacts the alpha (α) subunit of the heterotrimeric IL2 receptor complex, IL2Rαßγ, reducing its ability to bind and activate the heterotrimer. The IL2Rαßγ complex is constitutively expressed on regulatory T cells (Tregs). Therefore, without the use of mutations, PEGylation reduces the affinity for IL2Rαßγ to a greater extent than for IL2Rßγ, the receptor complex predominant on CD8 T cells. NKTR-214 treatment in vivo favors activation of CD8 T cells over Tregs in the tumor microenvironment to provide anti-tumor efficacy in multiple syngeneic models. Mechanistic modeling based on in vitro and in vivo kinetic data provides insight into the mechanism of NKTR-214 pharmacology. The model reveals that conjugated-IL2 protein derived from NKTR-214 occupy IL-2Rßγ to a greater extent compared to free-IL2 protein. The model accurately describes the sustained in vivo signaling observed after a single dose of NKTR-214 and explains how the properties of NKTR-214 impart a unique kinetically-controlled immunological mechanism of action.
[Mh] MeSH terms primary: Immunotherapy/methods
Interleukin-2/analogs & derivatives
Neoplasms/therapy
Polyethylene Glycols/pharmacology
Receptors, Interleukin-2/agonists
[Mh] MeSH terms secundary: Algorithms
Animals
CD8-Positive T-Lymphocytes/drug effects
CD8-Positive T-Lymphocytes/immunology
CD8-Positive T-Lymphocytes/metabolism
Cell Line, Tumor
Drug Liberation
Female
Interleukin Receptor Common gamma Subunit/agonists
Interleukin Receptor Common gamma Subunit/metabolism
Interleukin-2/pharmacokinetics
Interleukin-2/pharmacology
Interleukin-2 Receptor alpha Subunit/agonists
Interleukin-2 Receptor alpha Subunit/metabolism
Interleukin-2 Receptor beta Subunit/agonists
Interleukin-2 Receptor beta Subunit/metabolism
Kinetics
Mice, Inbred BALB C
Mice, Inbred C3H
Mice, Inbred C57BL
Models, Theoretical
Neoplasms/immunology
Neoplasms/metabolism
Phosphorylation/drug effects
Polyethylene Glycols/pharmacokinetics
Prodrugs/pharmacokinetics
Prodrugs/pharmacology
Receptors, Interleukin-2/metabolism
STAT5 Transcription Factor/metabolism
T-Lymphocytes, Regulatory/drug effects
T-Lymphocytes, Regulatory/immunology
T-Lymphocytes, Regulatory/metabolism
Transplantation, Homologous
Tumor Microenvironment/drug effects
Tumor Microenvironment/immunology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit); 0 (NKTR-214); 0 (Prodrugs); 0 (Receptors, Interleukin-2); 0 (STAT5 Transcription Factor); 30IQX730WE (Polyethylene Glycols)
[Em] Entry month:1710
[Cu] Class update date: 171006
[Lr] Last revision date:171006
[Js] Journal subset:IM
[Da] Date of entry for processing:170706
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179431

  10 / 2082 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 28657314
[Au] Autor:Quéméner A; Maillasson M; Arzel L; Sicard B; Vomiandry R; Mortier E; Dubreuil D; Jacques Y; Lebreton J; Mathé-Allainmat M
[Ad] Address:CRCINA, INSERM, CNRS, University of Nantes , Nantes 44007, France.
[Ti] Title:Discovery of a Small-Molecule Inhibitor of Interleukin 15: Pharmacophore-Based Virtual Screening and Hit Optimization.
[So] Source:J Med Chem;60(14):6249-6272, 2017 Jul 27.
[Is] ISSN:1520-4804
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interleukin (IL)-15 is a pleiotropic cytokine, which is structurally close to IL-2 and shares with it the IL-2 ß and γ receptor (R) subunits. By promoting the activation and proliferation of NK, NK-T, and CD8+ T cells, IL-15 plays important roles in innate and adaptative immunity. Moreover, the association of high levels of IL-15 expression with inflammatory and autoimmune diseases has led to the development of various antagonistic approaches targeting IL-15. This study is an original approach aimed at discovering small-molecule inhibitors impeding IL-15/IL-15R interaction. A pharmacophore and docking-based virtual screening of compound libraries led to the selection of 240 high-scoring compounds, 36 of which were found to bind IL-15, to inhibit the binding of IL-15 to the IL-2Rß chain or the proliferation of IL-15-dependent cells or both. One of them was selected as a hit and optimized by a structure-activity relationship approach, leading to the first small-molecule IL-15 inhibitor with sub-micromolar activity.
[Mh] MeSH terms primary: Interleukin-15/antagonists & inhibitors
Phthalazines/chemistry
Triazoles/chemistry
[Mh] MeSH terms secundary: Animals
Cell Line
Cell Proliferation/drug effects
Databases, Chemical
Humans
Interleukin-15/chemistry
Interleukin-15/metabolism
Interleukin-2 Receptor beta Subunit/chemistry
Interleukin-2 Receptor beta Subunit/metabolism
Mice
Molecular Docking Simulation
Phthalazines/chemical synthesis
Phthalazines/pharmacology
Small Molecule Libraries/chemistry
Stereoisomerism
Structure-Activity Relationship
Triazoles/chemical synthesis
Triazoles/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Interleukin-15); 0 (Interleukin-2 Receptor beta Subunit); 0 (Phthalazines); 0 (Small Molecule Libraries); 0 (Triazoles)
[Em] Entry month:1709
[Cu] Class update date: 170906
[Lr] Last revision date:170906
[Js] Journal subset:IM
[Da] Date of entry for processing:170629
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00485


page 1 of 209 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information