دورية أكاديمية

NFAT-Specific Inhibition by dNP2-VIVIT Ameliorates Autoimmune Encephalomyelitis by Regulation of Th1 and Th17

التفاصيل البيبلوغرافية
العنوان: NFAT-Specific Inhibition by dNP2-VIVIT Ameliorates Autoimmune Encephalomyelitis by Regulation of Th1 and Th17
المؤلفون: Hong-Gyun Lee, Li-Kyung Kim, Je-Min Choi
المصدر: Molecular Therapy: Methods & Clinical Development, Vol 16, Iss , Pp 32-41 (2020)
بيانات النشر: Elsevier, 2020.
سنة النشر: 2020
المجموعة: LCC:Genetics
LCC:Cytology
مصطلحات موضوعية: Genetics, QH426-470, Cytology, QH573-671
الوصف: Nuclear factor of activated T cells (NFATs) is an important transcription factor for T cell activation and proliferation. Recent studies have highlighted the role of NFATs in regulating the differentiation of effector CD4 T helper (Th) subsets including Th1 and Th17 cells. Because controlling the effector T cell function is important for the treatment of autoimmune diseases, regulation of NFAT functions in T cells would be an important strategy to control the pathogenesis of autoimmune diseases. Here, we demonstrated that an NFAT inhibitory peptide, VIVIT conjugated to dNP2 (dNP2-VIVIT), a blood-brain barrier-permeable peptide, ameliorated experimental autoimmune encephalomyelitis (EAE) by inhibiting Th1 and Th17 cells, but not regulatory T (Treg) cells. dNP2-VIVIT negatively regulated spinal cord-infiltrating interleukin-17A (IL-17A) and interferon (IFN)-γ-producing CD4+ T cells without affecting the number of Foxp3+ CD4+ Treg cells, whereas dNP2-VEET or 11R-VIVIT could not significantly inhibit EAE. In comparison with cyclosporin A (CsA), dNP2-VIVIT selectively inhibited Th1 and Th17 differentiation, whereas CsA inhibited the differentiation of all T cell subsets including that of Th2 and Treg cells. Collectively, this study demonstrated the role of dNP2-VIVIT as a novel agent for the treatment of autoimmune diseases such as multiple sclerosis by regulating the functions of Th1 and Th17 cells. Keywords: Multiple sclerosis (MS), VIVIT, T cell, Cell penetrating peptide (CPP), dNP2
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2329-0501
Relation: http://www.sciencedirect.com/science/article/pii/S2329050119301147; https://doaj.org/toc/2329-0501
DOI: 10.1016/j.omtm.2019.10.006
URL الوصول: https://doaj.org/article/d9511dc73f754005aabf2cf9f48a6895
رقم الأكسشن: edsdoj.9511dc73f754005aabf2cf9f48a6895
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:23290501
DOI:10.1016/j.omtm.2019.10.006