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

Kim DH, Ihn HJ, Moon C, Oh SS, Park S, Kim S, Lee KW, Kim KD - Biomol Ther (Seoul) (2015)

Bottom Line: In this study, we confirmed PPARγ-mediated inhibition of Th17 cell differentiation and cytokine production at an early stage.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea; ; PMBBRC, Gyeongsang National University, Jinju 660-701, Republic of Korea;

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.

No MeSH data available.


Related in: MedlinePlus

PPARγ ligands inhibit Th17 cells differentiation. (A) Naïve CD4+ T cells were purified and differentiated into Th17 cells with or without 25 μM of ciglitazone, rosiglitazone, and troglitazone. After 7 days, IL-17 producing CD4+ cells were analyzed using FACS. (B) Data from IL-17-producing cells with various concentrations of PPARγ ligand are indicated. One-way ANOVA was used for statistical analysis (p<0.01).
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f1-bt-23-71: PPARγ ligands inhibit Th17 cells differentiation. (A) Naïve CD4+ T cells were purified and differentiated into Th17 cells with or without 25 μM of ciglitazone, rosiglitazone, and troglitazone. After 7 days, IL-17 producing CD4+ cells were analyzed using FACS. (B) Data from IL-17-producing cells with various concentrations of PPARγ ligand are indicated. One-way ANOVA was used for statistical analysis (p<0.01).

Mentions: To confirm whether various PPARγ ligands could inhibit Th17 cell differentiation, we treated cells with PPARγ ligands (25 μM; Ciglitazone, Rosiglitazone, and Troglitazone) under conditions of Th17 cell differentiation for 7 days. The cells were subsequently stained with α-CD4 and α-IL-17 antibodies, and were analyzed for determination of Th17 cell differentiation. As shown in Fig. 1A., the PPARγ ligands inhibited Th17 cell differentiation. The inhibitory effect was dependent on the concentration of ligands, and ciglitazone and troglitazone were found to be more effective than rosiglitazone (Fig. 1B).


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

Kim DH, Ihn HJ, Moon C, Oh SS, Park S, Kim S, Lee KW, Kim KD - Biomol Ther (Seoul) (2015)

PPARγ ligands inhibit Th17 cells differentiation. (A) Naïve CD4+ T cells were purified and differentiated into Th17 cells with or without 25 μM of ciglitazone, rosiglitazone, and troglitazone. After 7 days, IL-17 producing CD4+ cells were analyzed using FACS. (B) Data from IL-17-producing cells with various concentrations of PPARγ ligand are indicated. One-way ANOVA was used for statistical analysis (p<0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4286752&req=5

f1-bt-23-71: PPARγ ligands inhibit Th17 cells differentiation. (A) Naïve CD4+ T cells were purified and differentiated into Th17 cells with or without 25 μM of ciglitazone, rosiglitazone, and troglitazone. After 7 days, IL-17 producing CD4+ cells were analyzed using FACS. (B) Data from IL-17-producing cells with various concentrations of PPARγ ligand are indicated. One-way ANOVA was used for statistical analysis (p<0.01).
Mentions: To confirm whether various PPARγ ligands could inhibit Th17 cell differentiation, we treated cells with PPARγ ligands (25 μM; Ciglitazone, Rosiglitazone, and Troglitazone) under conditions of Th17 cell differentiation for 7 days. The cells were subsequently stained with α-CD4 and α-IL-17 antibodies, and were analyzed for determination of Th17 cell differentiation. As shown in Fig. 1A., the PPARγ ligands inhibited Th17 cell differentiation. The inhibitory effect was dependent on the concentration of ligands, and ciglitazone and troglitazone were found to be more effective than rosiglitazone (Fig. 1B).

Bottom Line: In this study, we confirmed PPARγ-mediated inhibition of Th17 cell differentiation and cytokine production at an early stage.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.

View Article: PubMed Central - PubMed

Affiliation: Division of Applied Life Science, Gyeongsang National University, Jinju 660-701, Republic of Korea; ; PMBBRC, Gyeongsang National University, Jinju 660-701, Republic of Korea;

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.

No MeSH data available.


Related in: MedlinePlus