Peroxisome proliferator-activated receptors (PPARs) are members of a nuclear hormone receptor superfamily of ligand-activated transcriptional factors1 Recent data have shown that the prostaglandin ( PG), 152deoxy2-12,142PGJ2 (15d2PGJ2), and synthetic antidiabetic thiazolidinedione (TZDs), which are PPAR2γligands, suppress T cell proliferative response in vitro and inhibit inflammatory cytokine production by cells of monocyte/macrophage lineage11 Importantly, PPAR2γ ligands have been shown to ameliorate a variety of inflammatory conditions, including atherosclerosis, arthritis, inflammatory bowel disease and experimental autoimmune encephalomyelitis1-To explore the role of PPAR2γligands during the pathogenesis of experimental autoimmune myocarditis (EAM), we examined myocardial PPAR2γexpression in rats with EAM1 We also examined the effect of PPAR2γligands 15d2PGJ2 and plioglitazone on myocardial inflammation and on the expression of inflammatory cytokines1