• Anja Tautenhahn, Bernhard Brüne, and Andreas von Knethen.
• University of Kaiserslautern, Institute of Cell Biology, Erwin-Schroedinger-Strasse, Germany.
• J. Leukoc. Biol. 2003 May 1;73(5):665-72.

AbstractPhytohemagglutinin (PHA) elicited expression of peroxisome proliferator-activated receptor gamma (PPARgamma) in primary human T cells via the PPARgamma3 promoter, as shown by reverse transcription-polymerase chain reaction. Electrophoretic mobility shift assay demonstrated no correlation between PPARgamma expression and its activation. However, addition of specific PPARgamma agonists such as ciglitazone or 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) for 1 h following PHA pretreatment provoked PPARgamma activation verified by supershift analysis. Taking the proapoptotic properties of PPARgamma into consideration, we analyzed induction of apoptosis in activated T cells in response to PPARgamma agonists. Cells exposed to PPARgamma agonists alone revealed minor cell death compared with controls, whereas treatment with 15d-PGJ(2) or ciglitazone for 4 h subsequent to PHA stimulation significantly increased cell demise, which was attenuated by the pan-caspase inhibitor zVAD, pointing to apoptosis as the underlying mechanism. These data may be relevant for pathophysiological conditions accompanied with lymphopenia of T cells under conditions such as sepsis.

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