Ciglitazone, a Peroxisome Proliferator-Activated Receptor Gamma Ligand, Inhibits Proliferation and Differentiation of Th17 Cellsopen access
- Authors
- Kim, Dong Hyeok; Ihn, Hyun-ju; Moon, Chaerin; Oh, Sang-Seok; Park, Soojong; Kim, Suk; Lee, Keun Woo; Kim, Kwang Dong
- Issue Date
- 1-Jan-2015
- Publisher
- KOREAN SOC APPLIED PHARMACOLOGY
- Keywords
- Th17 cell; IL-17; PPAR gamma; CCNB1; Cell proliferation
- Citation
- BIOMOLECULES & THERAPEUTICS, v.23, no.1, pp.71 - 76
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- BIOMOLECULES & THERAPEUTICS
- Volume
- 23
- Number
- 1
- Start Page
- 71
- End Page
- 76
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/17467
- DOI
- 10.4062/biomolther.2014.042
- ISSN
- 1976-9148
- Abstract
- Peroxisome proliferator-activated receptor gamma (PPAR gamma) was identified as a cell-intrinsic regulator of Th17 cell differentiation. Th17 cells have been associated with several autoimmune diseases, including experimental autoimmune encephalomyelitis (EAE), inflammatory bowel disease (IBD), and collagen-induced arthritis. In this study, we confirmed PPAR gamma-mediated inhibition of Th17 cell differentiation and cytokine production at an early stage. Treatment with ciglitazone, a PPAR gamma ligand, reduced both IL-1 beta-mediated enhancement of Th17 differentiation and activation of Th17 cells after polarization. For Th17 cell differentiation, we found that ciglitazone-treated cells had a relatively low proliferative activity and produced a lower amount of cytokines, regardless of the presence of IL-1 beta. The inhibitory activity of ciglitazone might be due to decrease of CCNB1 expression, which regulates the cell cycle in T cells. Hence, we postulate that a pharmaceutical PPAR gamma activator might be a potent candidate for treatment of Th17-mediated autoimmune disease patients.
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