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231223s2011 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2010.10.004
|2 doi
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|a pubmed25n0678.xml
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|a (DE-627)NLM203320492
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|a (NLM)21044870
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Hjorth, Maria
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a GAD-alum treatment induces GAD65-specific CD4+CD25highFOXP3+ cells in type 1 diabetic patients
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1 |
|c 2011
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 08.03.2011
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|a Date Revised 03.12.2021
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2010 Elsevier Inc. All rights reserved.
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|a Type 1 diabetes results from autoimmune destruction of insulin producing pancreatic β-cells. We have shown that treatment with alum-formulated glutamic acid decarboxylase 65 (GAD-alum) preserved residual insulin secretion and induced antigen-specific responses in children with recent onset type 1 diabetes. The aim of this study was to further investigate the immunomodulatory effect of GAD-alum, focusing on CD4(+)CD25(high) cells and their association to cytokine secretion. Samples obtained 21 and 30months after the initial injection of GAD-alum or placebo were included in the present study. GAD(65)-stimulation enhanced the percentage of CD4(+)CD25(high)FOXP3(+) cells, but reduced the percentage of CD4(+)CD25(+) cells, in samples from the GAD-alum treated group. Further, the GAD(65)-induced secretion of IL-5, -10, and -13 correlated with the expression of CD4(+)CD25(high)FOXP3(+) cells, but inversely with CD4(+)CD25(+) cells. These new data suggest that GAD-alum treatment induced GAD(65)-specific T cells with regulatory features
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|a Journal Article
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|a Randomized Controlled Trial
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|a Research Support, Non-U.S. Gov't
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7 |
|a Alum Compounds
|2 NLM
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|a Autoantibodies
|2 NLM
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|a FOXP3 protein, human
|2 NLM
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| 650 |
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|a Forkhead Transcription Factors
|2 NLM
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| 650 |
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|a IL2RA protein, human
|2 NLM
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| 650 |
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|a Interleukin-2 Receptor alpha Subunit
|2 NLM
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| 650 |
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|a Interleukins
|2 NLM
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| 650 |
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|a Transforming Growth Factor beta
|2 NLM
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|a Tumor Necrosis Factor-alpha
|2 NLM
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| 650 |
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|a aluminum sulfate
|2 NLM
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| 650 |
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|a 34S289N54E
|2 NLM
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| 650 |
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|a Interferon-gamma
|2 NLM
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| 650 |
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7 |
|a 82115-62-6
|2 NLM
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| 650 |
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7 |
|a Glutamate Decarboxylase
|2 NLM
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| 650 |
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7 |
|a EC 4.1.1.15
|2 NLM
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| 650 |
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7 |
|a glutamate decarboxylase 2
|2 NLM
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| 650 |
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7 |
|a EC 4.1.1.15
|2 NLM
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| 700 |
1 |
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|a Axelsson, Stina
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Rydén, Anna
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Faresjö, Maria
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ludvigsson, Johnny
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Casas, Rosaura
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 138(2011), 1 vom: 07. Jan., Seite 117-26
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:138
|g year:2011
|g number:1
|g day:07
|g month:01
|g pages:117-26
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2010.10.004
|3 Volltext
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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| 952 |
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|d 138
|j 2011
|e 1
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|c 01
|h 117-26
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