Objective:　Recent　evidence　has　suggested　that　peroxisome　proliferator-activated　receptor-gamma　(PPAR-gamma)　serves　as　a　negative　regulator　in　the　immune　system.　In　the　present　study,　we　investigated　the　expression　of　PPAR-gamma　and　the　effect　of　PPAR-gamma　ligands　on　experimental　autoimmune　myocarditis　(EAM).　Methods　and　Results:　Experimental　autoimmune　myocarditis　was　induced　in　Lewis　rats　by　immunization　with　porcine　cardiac　myosin.　PPAR-gamma　ligands　15-deoxy-Delta(12,14)-PGJ(2)　200　mug　.　kg(-1).　d(-1)　by　ip　and　pioglitazone　10　mg　.　kg(-1)　.　d(-1)　by　oral　were　administered　for　3　weeks.　PPAR-gamma　expression　was　upregulated　in　myocarditis　and　the　enhanced　PPAR-gamma　expression　was　prominently　stained　in　the　nuclear　and　perinuclear　regions　of　the　positive-stained　cells　in　the　inflammatory　lesions.　Administration　of　PPAR-gamma　ligands　markedly　reduced　the　severity　of　myocarditis,　as　indicated　by　the　heart　weight/body　weight　ratio,　pericardial　effusion　scores,　macroscopic　scores,　and　microscopic　scores.　The　upregulated　PPAR-gamma　expression　was　also　reduced　by　PPAR-gamma　ligands　treatment.　In　addition,　PPAR-gamma　ligands　suppressed　the　proliferative　response　and　interferon-gamma　production　of　T　cell-enriched　splenocytes　from　rats　with　EAM.　Furthermore,　the　cytotoxic　activity　and　myocarditogenic　potential　of　these　T　cells　were　inhibited　by　PPAR-gamma　ligands　treatment.　Conclusions:　PPAR-gamma　ligands　ameliorate　EAM　associated　with　inhibition　of　expansion　and　activation　of　the　self-sensitive　T　cells.　These　results　suggest　that　PPAR-gamma　ligands　may　have　the　potential　to　modulate　human　inflammatory　heart　diseases　as　myocarditis.