NFAT-Specific Inhibition by dNP2-VIVIT Ameliorates Autoimmune Encephalomyelitis by Regulation of Th1 and Th17open access
- Authors
- Lee, Hong-Gyun; Kim, Li-Kyung; Choi, Je-Min
- Issue Date
- Mar-2020
- Publisher
- CELL PRESS
- Keywords
- Cell penetrating peptide (CPP); dNP2; Multiple sclerosis (MS); T cell; VIVIT
- Citation
- MOLECULAR THERAPY-METHODS & CLINICAL DEVELOPMENT, v.16, pp.32 - 41
- Indexed
- SCIE
SCOPUS
- Journal Title
- MOLECULAR THERAPY-METHODS & CLINICAL DEVELOPMENT
- Volume
- 16
- Start Page
- 32
- End Page
- 41
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/10649
- DOI
- 10.1016/j.omtm.2019.10.006
- Abstract
- 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 bloodbrain barrier-permeable peptide, ameliorated experimental autoimmune encephalomyelitis (EAE) by inhibiting Th 1 and Th17 cells, but not regulatory T (T-reg) cells. dNP2-VIVIT negatively regulated spinal cord-infiltrating interleukin-17A (IL17A) and interferon (IFN)-gamma-producing CD4(+ )T cells without affecting the number of Foxp3(+) CD4(+) T reg cells, whereas dNP2-VEET or 11R-VIVIT could not significantly inhibit EAE. In comparison with cyclosporin A (CsA), dNP2-VIVIT selectively inhibited Thl and Th17 differentiation, whereas CsA inhibited the differentiation of all T cell subsets including that of Th2 and T reg 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.
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