کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6087428 1207364 2015 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Oxidative stress and Treg depletion in lupus patients with anti-phospholipid syndrome
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Oxidative stress and Treg depletion in lupus patients with anti-phospholipid syndrome
چکیده انگلیسی


- Anti-phospholipid antibodies (APLA) are a diagnostic criterion of SLE.
- APLA cause anti-phospholipid syndrome (APS).
- Mitochondrial mass is increased in T cells of SLE patients with APS.
- Oxidative stress is increased in SLE patients with APS.
- Tregs are depleted in SLE patients with APS.

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinical Immunology - Volume 158, Issue 2, June 2015, Pages 148-152
نویسندگان
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