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Expression by Peroxisome Proliferator-Activated Receptor 1
,
* Research Service and Division of Nephrology-Hypertension, Veterans Affairs San Diego Healthcare System, San Diego, CA 92161; and
Departments of Cellular and Molecular Medicine and
Medicine, University of California, San Diego, CA 92093
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors expressed in a wide variety of cells. Our studies and others have demonstrated that both human and murine T cells express PPAR
and that expression can be augmented over time in mitogen-activated splenocytes. PPAR ligands decrease proliferation and IL-2 production, and induce apoptosis in both B and T cells. PPAR ligands have also been shown to be anti-inflammatory in multiple models of inflammatory disease. In the following study, we demonstrate for the first time that PPAR is expressed in both murine CD4 and CD8 cells and that PPAR ligands directly decrease IFN- expression by murine and transformed T cell lines. Unexpectedly, GW9662, a PPAR antagonist, increases lymphocyte IFN- expression. Transient transfection studies reveal that PPAR ligands, in a PPAR-dependent manner, potently repress an IFN- promoter construct. Repression localizes to the distal conserved sequence of the IFN- promoter. Our studies also demonstrate that PPAR acts on the IFN- promoter by interfering with c-Jun activation. These studies suggest that many of the observed anti-inflammatory effects of PPAR ligands may be related to direct inhibition of IFN- by PPAR.
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