کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
7280545 | 1473915 | 2016 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Antibodies to β adrenergic and muscarinic cholinergic receptors in patients with Chronic Fatigue Syndrome
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کلمات کلیدی
CFSautoantibodiesGPCRAChRTPOADRPOTSG-protein coupled receptor - G-پروتئین همراه گیرندهanti-nuclear antibodies - آنتی بادی های ضد هسته ایANA - اصلیRituximab - ریتوکسیمابPostural orthostatic tachycardia syndrome - سندرم تاتکاردی ارتوپلاستیک موضعیChronic fatigue syndrome - سندرم خستگی مزمن، سندروم خستگی مفرطRecurrent respiratory tract infections - عفونت های تنفسی مجددacetylcholine receptor - گیرنده استیل کولینAdrenergic receptors - گیرنده های آدرنرژیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Infection-triggered disease onset, chronic immune activation and autonomic dysregulation in CFS point to an autoimmune disease directed against neurotransmitter receptors. Autoantibodies against G-protein coupled receptors were shown to play a pathogenic role in several autoimmune diseases. Here, serum samples from a patient cohort from Berlin (n = 268) and from Bergen with pre- and post-treatment samples from 25 patients treated within the KTS-2 rituximab trial were analysed for IgG against human α and β adrenergic, muscarinic (M) 1-5 acetylcholine, dopamine, serotonin, angiotensin, and endothelin receptors by ELISA and compared to a healthy control cohort (n = 108). Antibodies against β2, M3 and M4 receptors were significantly elevated in CFS patients compared to controls. In contrast, levels of antibodies against α adrenergic, dopamine, serotonin, angiotensin, and endothelin receptors were not different between patients and controls. A high correlation was found between levels of autoantibodies and elevated IgG1-3 subclasses, but not with IgG4. Further patients with high β2 antibodies had significantly more frequently activated HLA-DR+ T cells and more frequently thyreoperoxidase and anti-nuclear antibodies. In patients receiving rituximab maintenance treatment achieving prolonged B-cell depletion, elevated β2 and M4 receptor autoantibodies significantly declined in clinical responder, but not in non-responder. We provide evidence that 29.5% of patients with CFS had elevated antibodies against one or more M acetylcholine and β adrenergic receptors which are potential biomarkers for response to B-cell depleting therapy. The association of autoantibodies with immune markers suggests that they activate B and T cells expressing β adrenergic and M acetylcholine receptors. Dysregulation of acetylcholine and adrenergic signalling could also explain various clinical symptoms of CFS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain, Behavior, and Immunity - Volume 52, February 2016, Pages 32-39
Journal: Brain, Behavior, and Immunity - Volume 52, February 2016, Pages 32-39
نویسندگان
Madlen Loebel, Patricia Grabowski, Harald Heidecke, Sandra Bauer, Leif G. Hanitsch, Kirsten Wittke, Christian Meisel, Petra Reinke, Hans-Dieter Volk, Ãystein Fluge, Olav Mella, Carmen Scheibenbogen,