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(Journal of Leukocyte Biology. 2003;73:665-672.)
© 2003 by Society for Leukocyte Biology

Activation-induced PPAR expression sensitizes primary human T cells toward apoptosis

University of Kaiserslautern, Institute of Cell Biology, Erwin-Schroedinger-Strasse, Germany

Correspondence: Andreas von Knethen, University of Kaiserslautern, Institute of Cell Biology, Erwin-Schroedinger-Strasse 13/420A, 67663 Kaiserslautern, Germany. E-mail: aknethen{at}rhrk.uni-kl.de

Phytohemagglutinin (PHA) elicited expression of peroxisome proliferator-activated receptor (PPAR) in primary human T cells via the PPAR3 promoter, as shown by reverse transcription-polymerase chain reaction. Electrophoretic mobility shift assay demonstrated no correlation between PPAR expression and its activation. However, addition of specific PPAR agonists such as ciglitazone or 15-deoxy-^12,14-prostaglandin J₂ (15d-PGJ₂) for 1 h following PHA pretreatment provoked PPAR activation verified by supershift analysis. Taking the proapoptotic properties of PPAR into consideration, we analyzed induction of apoptosis in activated T cells in response to PPAR agonists. Cells exposed to PPAR agonists alone revealed minor cell death compared with controls, whereas treatment with 15d-PGJ₂ 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.

Key Words: inflammation • lymphocyte • cell death

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