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231224s2015 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2015.03.024
|2 doi
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|a pubmed24n0826.xml
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|a (DE-627)NLM247945056
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|a (NLM)25862984
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|a (PII)S1521-6616(15)00127-8
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Lai, Zhi-wei
|e verfasserin
|4 aut
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|a Oxidative stress and Treg depletion in lupus patients with anti-phospholipid syndrome
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|c 2015
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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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|a Date Completed 25.08.2015
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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 © 2015 Elsevier Inc. All rights reserved.
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|a Anti-phospholipid antibodies (APLA) represent a diagnostic criterion of systemic lupus erythematosus (SLE) and cause morbidity, termed anti-phospholipid syndrome (APS). Activation of the mechanistic target of rapamycin (mTOR) has been recently associated with APS. mTOR is a sensor of oxidative stress. Therefore, we examined mitochondrial mass, superoxide production, mTOR activity and FoxP3 expression in 72 SLE patients, twelve of whom also had APS, and 54 healthy controls by flow cytometry. Mitochondrial mass was increased in CD4(-)CD8(-) double-negative (DN) T cells of SLE patients with APS (2.7-fold) in comparison to those without APS (1.7-fold; p = 0.014). Superoxide production was increased in all lymphocyte subsets of APS patients. FoxP3(+) cells were depleted within CD4(+)CD25(+) Tregs in patients with APS (28.4%) relative to those without APS (46.3%, p = 0.008). mTOR activity was similar between SLE patients with and without APS. Thus, oxidative stress and Treg depletion rather than mTOR activation underlie APS in patients with SLE
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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 Anti-phospholipid syndrome
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|a Mechanistic target of rapamycin
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|a Oxidative stress
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|a Systemic lupus erythematosus
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|a Treg
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|a mTOR
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|a Biomarkers
|2 NLM
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|a Multiprotein Complexes
|2 NLM
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|a Mechanistic Target of Rapamycin Complex 1
|2 NLM
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|a EC 2.7.11.1
|2 NLM
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|a TOR Serine-Threonine Kinases
|2 NLM
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|a EC 2.7.11.1
|2 NLM
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1 |
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|a Marchena-Mendez, Ivan
|e verfasserin
|4 aut
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1 |
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|a Perl, Andras
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 158(2015), 2 vom: 01. Juni, Seite 148-52
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:158
|g year:2015
|g number:2
|g day:01
|g month:06
|g pages:148-52
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|u http://dx.doi.org/10.1016/j.clim.2015.03.024
|3 Volltext
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