Ginsenoside Re enhances survival of human CD4<SUP>+</SUP> T cells through regulation of autophagy
- Authors
- Son, Young Min; Kwak, Chae Won; Lee, Yeo Jin; Yang, Deok-Chun; Park, Byung-Chul; Lee, Woon Kyu; Han, Seung Hyun; Yun, Cheol-Heui
- Issue Date
- May-2010
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Ginsenoside Re; CD4(+) T cells; Autophagy; Interferon related GTPase family M; Interferon-gamma
- Citation
- INTERNATIONAL IMMUNOPHARMACOLOGY, v.10, no.5, pp 626 - 631
- Pages
- 6
- Journal Title
- INTERNATIONAL IMMUNOPHARMACOLOGY
- Volume
- 10
- Number
- 5
- Start Page
- 626
- End Page
- 631
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/72139
- DOI
- 10.1016/j.intimp.2010.03.002
- ISSN
- 1567-5769
1878-1705
- Abstract
- In the present study, we examined the effects of ginsenoside Re (Re) on cytokine expression, cytokine-dependent autophagy and cell survival in human CD4(+) T cells. When CD4(+) T cells isolated from human peripheral blood were treated with Re, LC3 and monodansylcadaverine (MDC), representative markers of autophagy, were decreased in a dose-dependent manner. Interestingly, Re suppressed the production of interferon-gamma (IFN-gamma) and immunity-related GTPase family M (IRGM) in CD4(+) T cells whereas no changes in other autophagy-related signaling molecules (ERK, p38 and AKT-mTOR-p70S6k) were found. Concomitantly, we observed that Re increased the proliferation of CD4(+) T cells with decreased cell death. Our results demonstrate that ginsenoside Re enhanced viability of CD4(+) T cells through the regulation of IFN-gamma-dependent autophagy activity. (C) 2010 Elsevier B.V. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Biotechnology & Natural Resource > Department of Systems Biotechnology > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/72139)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.