Parkinson’s disease (PD) is a chronic, age related neurodegenerative disease. Evidence is accumulating that a number of genetic and environmental factors are involved in the pathogenesis of PD, leading to mitochondrial dysfunction, neuroinflammation or autoimmunity. We have obtained evidence that DJ-1, a familial Parkinson’s disease gene, plays a key role in the differentiation and function of regulatory T cells. We were able to show that DJ-1 directly binds to PDH-E1 beta (PDHB) subunit of the pyruvate dehydrogenase complex, a central switch between glycolysis and oxidative phosphorylation. DJ-1 depletion impaired Treg proliferation and cellularity in older but not younger mice and increased the severity of experimental autoimmune encephalomyelitis (EAE) during the remission phase. Based on the central nature of PDH in controlling central energy metabolism and biosynthesis, I will discuss potential implications of cellular energetics for other chronic diseases, e.g. diabetes, inflammation or cancer.