PPAR-γ ligands inhibit the expression of inflammatory cytokines and attenuate autoimmune myocarditis

Peroxisome proliferator-activated receptors (PPARs) are members of a nuclear hormone receptor superfamily of ligand-activated transcriptional factors. Recent data have shown that the prostaglandin (PG), 15-deoxy-△12,14-PGJ2 (15d-PGJ2), and synthetic antidiabetic thiazolidinedione (TZDs), which are PPAR-γ ligands, suppress T cell proliferative response in vitro and inhibit inflammatory cytokine production by cells of monocyte/macrophage lineage.1 Importantly, PPAR-γ ligands have been shown to ameliorate a variety of inflammatory conditions, including atherosclerosis, arthritis, inflammatory bowel disease and experimental autoimmune encephalomyelitis.2