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Article

Crosstalk between PPARγ Ligands and Inflammatory-Related Pathways in Natural T-Regulatory Cells from Type 1 Diabetes Mouse Model

1
School of Health Sciences, Universiti Sains Malaysia, Kelantan, Kubang Kerian 16150, Malaysia
2
Regenerative Medicine Cluster, Advanced Medical and Dental Institute (AMDI), Universiti Sains Malaysia, Bertam, Kepala Batas 13200, Malaysia
3
School of Medical Sciences, Universiti Sains Malaysia, Kelantan, Kubang Kerian 16150, Malaysia
*
Authors to whom correspondence should be addressed.
Biomolecules 2018, 8(4), 135; https://doi.org/10.3390/biom8040135
Received: 21 June 2018 / Revised: 24 August 2018 / Accepted: 28 August 2018 / Published: 5 November 2018
Immunomodulation, as a means of immunotherapy, has been studied in major research and clinical laboratories for many years. T-Regulatory (Treg) cell therapy is one of the modulators used in immunotherapy approaches. Similarly, nuclear receptor peroxisome proliferator activated receptor gamma (PPARγ) has extensively been shown to play a role as an immuno-modulator during inflammation. Given their mutual roles in downregulating the immune response, current study examined the influence of PPARγ ligands i.e., thiazolidinedione (TZD) class of drugs on Forkhead Box P3 (Foxp3) expression and possible crosstalk between PPARγ and nTreg cells of Non-Obese Diabetes (NOD) and Non-Obese Diabetes Resistant (NOR) mice. Results showed that TZD drug, ciglitazone and natural ligand of PPARγ 15d-prostaglandin downregulated Foxp3 expression in activated nTreg cells from both NOD and NOR mice. Interestingly, addition of the PPARγ inhibitor, GW9662 further downregulated Foxp3 expression in these cells from both mice. We also found that PPARγ ligands negatively regulate Foxp3 expression in activated nTreg cells via PPARγ-independent mechanism(s). These results demonstrate that both natural and synthetic PPARγ ligands capable of suppressing Foxp3 expression in activated nTreg cells of NOD and NOR mice. This may suggest that the effect of PPARγ ligands in modulating Foxp3 expression in activated nTreg cells is different from their reported effects on effector T cells. Given the capability to suppress Foxp3 gene, it is possible to be tested as immunomodulators in cancer-related studies. The co-lateral use of PPARγ ligands in nTreg cells in inducing tolerance towards pseudo-self antigens as in tumor microenvironment may uphold beneficial outcomes. View Full-Text
Keywords: T-Regulatory cells; immune regulation; Foxp3; PPARγ; autoimmune diabetes; NOD mouse; thiazolidinediones; ciglitazone; immunomodulator T-Regulatory cells; immune regulation; Foxp3; PPARγ; autoimmune diabetes; NOD mouse; thiazolidinediones; ciglitazone; immunomodulator
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MDPI and ACS Style

Nor Effa, S.Z.; Yaacob, N.S.; Mohd Nor, N. Crosstalk between PPARγ Ligands and Inflammatory-Related Pathways in Natural T-Regulatory Cells from Type 1 Diabetes Mouse Model. Biomolecules 2018, 8, 135. https://doi.org/10.3390/biom8040135

AMA Style

Nor Effa SZ, Yaacob NS, Mohd Nor N. Crosstalk between PPARγ Ligands and Inflammatory-Related Pathways in Natural T-Regulatory Cells from Type 1 Diabetes Mouse Model. Biomolecules. 2018; 8(4):135. https://doi.org/10.3390/biom8040135

Chicago/Turabian Style

Nor Effa, S. Z., Nik S. Yaacob, and Norazmi Mohd Nor. 2018. "Crosstalk between PPARγ Ligands and Inflammatory-Related Pathways in Natural T-Regulatory Cells from Type 1 Diabetes Mouse Model" Biomolecules 8, no. 4: 135. https://doi.org/10.3390/biom8040135

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