Uncoupling protein UCP2: When mitochondrial activity meets immunity

• Published in: FEBS letters 2010-04, Vol.584 (8), p.1437-1442
• Main Authors: Emre, Yalin, Nübel, Tobias
• Format: Article
• Language: English
• Subjects: Animals; EAE; experimental autoimmune encephalomyelitis; Genomics; Humans; IFN; IFN-inducible protein 10; Immune response; Immunity; inducible nitric oxide synthase; Inflammation; iNOS; interferon; interleukin; Ion Channels - deficiency; Ion Channels - metabolism; IP10; knock out; lipopolysaccharide; LPS; Macrophages - immunology; Macrophages - metabolism; MCP1; MIG; Mitochondria; Mitochondria - metabolism; Mitochondrial Proteins - deficiency; Mitochondrial Proteins - metabolism; MOG; monocyte chemotactic protein-1; monokine induced by IFN-γ; myelin oligodendrocyte glycoprotein; nitric oxide; peroxisome proliferator-activated receptor-gamma coactivator; PGC; Reactive oxygen species; ROS; Signal Transduction; TLR; TNF; Toll-like receptor; tumor necrosis factor; UCP; uncoupling protein; Uncoupling Protein 2; Wild-type
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2010.03.014

Uncoupling protein 2 (UCP2) belongs to the family of mitochondrial carriers. Here, we highlight recent findings regarding UCP2 function in the immune system. UCP2 controls immune cell activation by modulating MAPK pathways and the production of mitochondrial reactive oxygen species. In several models of infection, inflammation and autoimmunity, a regulatory impact of UCP2 was demonstrated by its direct implication in the production of cytokines and nitric oxide and in cell migration. In addition, UCP2 is reported as a key protein for oxidation of fatty acids, glutamine and glucose. Therefore we present a model of how the regulation of nutrient oxidation by UCP2 promotes immune cell activation.