2. Academic Validation
  3. Ciglitazone, a peroxisome proliferator-activated receptor gamma ligand, inhibits proliferation and differentiation of th17 cells

Ciglitazone, a peroxisome proliferator-activated receptor gamma ligand, inhibits proliferation and differentiation of th17 cells

  • Biomol Ther (Seoul). 2015 Jan;23(1):71-6. doi: 10.4062/biomolther.2014.042.
Dong Hyeok Kim 1,  Hyun-Ju Ihn 2,  Chaerin Moon 2,  Sang-Seok Oh 3,  Soojong Park 3,  Suk Kim 4,  Keun Woo Lee 5,  Kwang Dong Kim 1
Affiliations

Affiliations

  • 1 Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea; ; PMBBRC, Gyeongsang National University, Jinju 660-701, Republic of Korea;
  • 2 Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea;
  • 3 Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea; ; BK21 Plus, Gyeongsang National University, Jinju 660-701, Republic of Korea;
  • 4 College of Veterinary Medicine, Gyeongsang National University, Jinju 660-701, Republic of Korea.
  • 5 Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea; ; BK21 Plus, Gyeongsang National University, Jinju 660-701, Republic of Korea; ; PMBBRC, Gyeongsang National University, Jinju 660-701, Republic of Korea;
PMID: 25593646 DOI: 10.4062/biomolther.2014.042
Abstract

Peroxisome Proliferator-activated Receptor gamma (PPARγ) 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 PPARγ-mediated inhibition of Th17 cell differentiation and cytokine production at an early stage. Treatment with ciglitazone, a PPARγ ligand, reduced both IL-1β-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-1β. 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 PPARγ Activator might be a potent candidate for treatment of Th17-mediated autoimmune disease patients.

Keywords

CCNB1; Cell proliferation; IL-17; PPARγ; Th17 cell.

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