کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3065054 | 1580464 | 2009 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Suppression of experimental autoimmune myasthenia gravis by inhibiting the signaling between IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
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چکیده انگلیسی
We have previously demonstrated that the chemokine IFN-γ inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 209, Issues 1–2, 30 April 2009, Pages 87–95
Journal: Journal of Neuroimmunology - Volume 209, Issues 1–2, 30 April 2009, Pages 87–95
نویسندگان
Tali Feferman, Revital Aricha, Keren Mizrachi, Erez Geron, Ronen Alon, Miriam. C. Souroujon, Sara Fuchs,