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Ciglitazone, a Peroxisome Proliferator-Activated Receptor Gamma Ligand, Inhibits Proliferation and Differentiation of Th17 Cells

  • Kim, Dong Hyeok (Division of Applied Life Science, Gyeongsang National University) ;
  • Ihn, Hyun-Ju (Division of Applied Life Science, Gyeongsang National University) ;
  • Moon, Chaerin (Division of Applied Life Science, Gyeongsang National University) ;
  • Oh, Sang-Seok (Division of Applied Life Science, Gyeongsang National University) ;
  • Park, Soojong (Division of Applied Life Science, Gyeongsang National University) ;
  • Kim, Suk (College of Veterinary Medicine, Gyeongsang National University) ;
  • Lee, Keun Woo (Division of Applied Life Science, Gyeongsang National University) ;
  • Kim, Kwang Dong (Division of Applied Life Science, Gyeongsang National University)
  • Received : 2014.04.14
  • Accepted : 2014.10.07
  • Published : 2015.01.01

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.

Keywords

References

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