کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10940769 | 1095508 | 2016 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increased expression of Toll-like receptors 7 and 9 in myasthenia gravis thymus characterized by active Epstein-Barr virus infection
ترجمه فارسی عنوان
افزایش بیان گره های 7 و 9 مانند درمستونیا گراویوس تیموس به واسطه عفونت ویروس اپشتاین بار
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
AChRRIG-ILMP1IRF8retinoic acid inducible gene-IEBERTLRMDCDAPITECLCMPDC4′,6-diamidino-2-phenylindole, dihydrochloride - 4 '، 6-دیامیدینو-2-فنیلینول، دی هیدروکلرایدRheumatoid arthritis - آرتریتروماتوئیدEBV - اپشتین بار ویروسinterferon - اینترفرونIFN - اینترفرون هاThymus - تیموسToll-like receptor - تیالآرPlasmacytoid dendritic cell - سلول دندریتیک پلاسماییکوئیدThymic epithelial cells - سلول های اپیتلیال ThymicMyeloid dendritic cell - سلول های دندریتیک میلوئیدinterferon regulatory factor 8 - عامل تنظیمی اینترفرون 8Systemic lupus erythematosus - لوپوس اریتماتوی سیستمیکSLE - لوپوس منتشر یا لوپوس اریتماتوس سیستمیکLaser-capture microdissection - لیزر جذب microdissectionGerminal center - مرکز ژرمینالMyasthenia gravis - میاستنی گراویسEpstein–Barr virus - ویروس Epstein-Barracetylcholine receptor - گیرنده استیل کولینtoll-like receptor 7 - گیرنده شماره 7Toll-like receptor 9 - گیرنده پولی مانند 9
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
چکیده انگلیسی
Considerable data implicate the thymus as the main site of autosensitization to the acetylcholine receptor in myasthenia gravis (MG), a B-cell-mediated autoimmune disease affecting the neuromuscular junction. We recently demonstrated an active Epstein-Barr virus (EBV) infection in the thymus of MG patients, suggesting that EBV might contribute to the onset or maintenance of the autoimmune response within MG thymus, because of its ability to activate and immortalize autoreactive B cells. EBV has been reported to elicit and modulate Toll-like receptor (TLR) 7- and TLR9-mediated innate immune responses, which are known to favor B-cell dysfunction and autoimmunity. Aim of this study was to investigate whether EBV infection is associated with altered expression of TLR7 and TLR9 in MG thymus. By real-time PCR, we found that TLR7 and TLR9 mRNA levels were significantly higher in EBV-positive MG compared to EBV-negative normal thymuses. By confocal microscopy, high expression levels of TLR7 and TLR9 proteins were observed in B cells and plasma cells of MG thymic germinal centers (GCs) and lymphoid infiltrates, where the two receptors co-localized with EBV antigens. An increased frequency of Ki67-positive proliferating B cells was found in MG thymuses, where we also detected proliferating cells expressing TLR7, TLR9 and EBV antigens, thus supporting the idea that EBV-associated TLR7/9 signaling may promote abnormal B-cell activation and proliferation. Along with B cells and plasma cells, thymic epithelium, plasmacytoid dendritic cells and macrophages exhibited enhanced TLR7 and TLR9 expression in MG thymus; TLR7 was also increased in thymic myeloid dendritic cells and its transcriptional levels positively correlated with those of interferon (IFN)-β. We suggested that TLR7/9 signaling may be involved in antiviral type I IFN production and long-term inflammation in EBV-infected MG thymuses. Our overall findings indicate that EBV-driven TLR7- and TLR9-mediated innate immune responses may participate in the intra-thymic pathogenesis of MG.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 221, Issue 4, April 2016, Pages 516-527
Journal: Immunobiology - Volume 221, Issue 4, April 2016, Pages 516-527
نویسندگان
Paola Cavalcante, Barbara Galbardi, Sara Franzi, Stefania Marcuzzo, Claudia Barzago, Silvia Bonanno, Giorgia Camera, Lorenzo Maggi, Dimos Kapetis, Francesca Andreetta, Amelia Biasiucci, Teresio Motta, Carmelo Giardina, Carlo Antozzi, Fulvio Baggi,