An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56(bright) NK cells. - Wikidata - wikimedia - TriplyDB

An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56(bright) NK cells.

An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56(bright) NK cells.

http://www.wikidata.org/entity/Q34893862

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Cellular targeting in autoimmunity Application of IL-2 therapy to target T regulatory cell function Daclizumab therapy for multiple sclerosis Therapeutic efficacy of monthly subcutaneous injection of daclizumab in relapsing multiple sclerosis A pilot study of IL-2Rα blockade during lymphopenia depletes regulatory T-cells and correlates with enhanced immunity in patients with glioblastoma The effects of interleukin-2 on immune response regulation.The efficacy and safety of daclizumab and its potential role in the treatment of multiple sclerosis.Daclizumab high-yield process in the treatment of relapsing-remitting multiple sclerosis How implementation of systems biology into clinical trials accelerates understanding of diseases.Interleukin-2/interleukin-2 antibody therapy induces target organ natural killer cells that inhibit central nervous system inflammation.A role for interleukin-2 trans-presentation in dendritic cell-mediated T cell activation in humans, as revealed by daclizumab therapy.CD56(bright) natural killer cells and response to daclizumab HYP in relapsing-remitting MS Central role for interleukin-2 in type 1 diabetes.Daclizumab reverses intrathecal immune cell abnormalities in multiple sclerosis What do effective treatments for multiple sclerosis tell us about the molecular mechanisms involved in pathogenesis?Patients with MS under daclizumab therapy mount normal immune responses to influenza vaccination CNS vasculitis in a patient with MS on daclizumab monotherapy Cutaneous adverse events in multiple sclerosis patients treated with daclizumab Impaired NK-mediated regulation of T-cell activity in multiple sclerosis is reconstituted by IL-2 receptor modulation Inhibition of LTi cell development by CD25 blockade is associated with decreased intrathecal inflammation in multiple sclerosis.Effect of daclizumab high-yield process in patients with highly active relapsing-remitting multiple sclerosis.Multi-cellular natural killer (NK) cell clusters enhance NK cell activation through localizing IL-2 within the cluster.Daclizumab-induced adverse events in multiple organ systems in multiple sclerosis.Teriflunomide and its mechanism of action in multiple sclerosis.The role of natural killer cells in multiple sclerosis and their therapeutic implications.Monoclonal antibodies in neuroinflammatory diseases.Modulation of IL-2Rα with daclizumab for treatment of multiple sclerosis.Novel monoclonal antibodies for therapy of multiple sclerosis.Daclizumab for the treatment of multiple sclerosis.Monoclonal Antibodies for Relapsing Multiple Sclerosis: A Review of Recently Marketed and Late-Stage Agents.Human CD56bright NK Cells: An Update.Therapeutic Application of Monoclonal Antibodies in Multiple Sclerosis.The two-pore domain K2 P channel TASK2 drives human NK-cell proliferation and cytolytic function.Impact of Immune-Modulatory Drugs on Regulatory T Cell.A role for pre-mNK cells in tumor progression.Regulatory Functions of Natural Killer Cells in Multiple Sclerosis.Daclizumab: A Review in Relapsing Multiple Sclerosis.Daclizumab for the treatment of relapsing-remitting multiple sclerosis.Production and characterization of a CD25-specific scFv-Fc antibody secreted from Pichia pastoris.Daclizumab: Development, Clinical Trials, and Practical Aspects of Use in Multiple Sclerosis.

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An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56(bright) NK cells.

http://www.wikidata.org/entity/Q34893862

description

2010 nî lūn-bûn

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2010 թուականի Յունիսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հունիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56

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An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

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An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

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type

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An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56

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An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

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An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

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prefLabel

An IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56

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An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

@ast

An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

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JIMMUNOL.0902238

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Journal of Immunology

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An IL-2 paradox: blocking CD25 ...... tion of CD56(bright) NK cells.

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Bibiana Bielekova

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Jayne F Martin

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Justin S A Perry

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Neha R Jakhete

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Xiang Wang

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P2860

Structure of the quaternary complex of interleukin-2 with its alpha, beta, and gammac receptors

Risk alleles for multiple sclerosis identified by a genomewide study

IL-2 negatively regulates IL-7 receptor alpha chain expression in activated T lymphocytes.

Humanized anti-CD25 (daclizumab) inhibits disease activity in multiple sclerosis patients failing to respond to interferon beta

Regulatory CD56(bright) natural killer cells mediate immunomodulatory effects of IL-2Ralpha-targeted therapy (daclizumab) in multiple sclerosis.

The IL-2/IL-15 receptor systems: targets for immunotherapy.

Daclizumab phase II trial in relapsing and remitting multiple sclerosis: MRI and clinical results.

Potential mechanisms of human natural killer cell expansion in vivo during low-dose IL-2 therapy.

Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells

Treatment of noninfectious intermediate and posterior uveitis with the humanized anti-Tac mAb: a phase I/II clinical trial.

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