کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3060745 1187456 2011 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Interleukin-17-secreting T cells in neuromyelitis optica and multiple sclerosis during relapse
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی عصب شناسی
پیش نمایش صفحه اول مقاله
Interleukin-17-secreting T cells in neuromyelitis optica and multiple sclerosis during relapse
چکیده انگلیسی

Growing evidence suggests that interleukin (IL)-17 and IL-17-secreting CD4+T (Th17) cells are involved in the pathogenic mechanisms of multiple sclerosis (MS). IL-17-secreting CD8+T cells were recently identified as a novel subset of CD8+T cells. We aimed to analyze the role of Th17 and IL-17 secreting CD8+T cells in the pathogenesis of neuromyelitis optica (NMO) as well as MS. Fourteen patients with NMO, 20 with MS and 16 control participants (CTL) were enrolled between November 2008 and December 2009. The proportion of Th17 cells and IL-17 secreting CD8+T cells were counted using flow cytometry, and serum levels of IL-6, IL-17, IL-21, IL-23, and transforming growth factor-beta (TGF-β) were measured by enzyme-linked immunosorbent assay. Patients with NMO had a larger proportion of Th17 cells than patients with MS (3.72% versus [vs.] 2.58%, p = 0.02) and CTL (3.72% vs. 1.36%, p < 0.001). The proportion of Th17 cells in patients with MS was also markedly higher than in the CTL (2.58% vs. 1.36%, p < 0.001). IL-17-secreting CD8+T cell counts in NMO patients were markedly higher than in MS patients (1.61% vs. 1.09%, p = 0.036) and CTLs (1.61% vs. 0.58%, p < 0.001). The proportion of IL-17-secreting CD8+T cells in MS patients was also higher than in CTLs (1.09% vs. 0.58%, p = 0.002). Serum IL-17 and IL-23 levels were increased in patients with NMO and MS, while serum IL-21 concentration was higher only in NMO patients compared to CTL. We concluded that Th17 cells were highly activated in patients with NMO. IL-17-secreting CD8+T cells were increased in patients with NMO and MS during relapse and have an important role in the pathological mechanism of NMO and MS.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Clinical Neuroscience - Volume 18, Issue 10, October 2011, Pages 1313–1317
نویسندگان
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