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231223s2011 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2010.12.006
|2 doi
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|a pubmed24n0685.xml
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|a (NLM)21276756
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|a DE-627
|b ger
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|e rakwb
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|a eng
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|a Crowder, Roslyn N
|e verfasserin
|4 aut
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|a B lymphocytes are resistant to death receptor 5-induced apoptosis
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|c 2011
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
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|a ƒa Online-Ressource
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|a Date Completed 01.06.2011
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|a Date Revised 20.10.2021
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Published by Elsevier Inc.
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|a Death Receptor 5 (DR5) induces apoptosis in various types of cells and is a potential therapeutic target. We have investigated whether targeting DR5 could be used to eliminate pathogenic B lymphocytes from systemic lupus erythematosus (SLE) patients. We examined DR5 expression and function on B lymphocytes from healthy controls subjects, SLE patients, and human tonsil. DR5 was expressed similarly on all B cell subpopulations, including resting and activated B cells. Expression of DR5 was equivalent on B cells from SLE patients and healthy subjects. Additionally, DR5 expression was unchanged after B lymphocyte stimulation. However, B cells were resistant to DR5-induced apoptosis, including after in vitro activation. No changes in subsets of B cells were observed in subjects of a trial of CS-1008, an agonist anti-DR5. While DR5 shows promise as a way to selectively eliminate tumor cells and activated synoviocytes, these data suggest DR5 alone cannot be used as a target to remove pathogenic SLE B cells
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|a Journal Article
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|a Research Support, N.I.H., Extramural
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|a Research Support, Non-U.S. Gov't
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|a Antibodies, Monoclonal
|2 NLM
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|a Receptors, TNF-Related Apoptosis-Inducing Ligand
|2 NLM
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|a Zhao, Hong
|e verfasserin
|4 aut
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|a Chatham, W Winn
|e verfasserin
|4 aut
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|a Zhou, Tong
|e verfasserin
|4 aut
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|a Carter, Robert H
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 139(2011), 1 vom: 08. Apr., Seite 21-31
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:139
|g year:2011
|g number:1
|g day:08
|g month:04
|g pages:21-31
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|u http://dx.doi.org/10.1016/j.clim.2010.12.006
|3 Volltext
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