deletion of ucp2 in inos deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis删除ucp2在伊诺缺乏小鼠实验性自身免疫性脑脊髓炎期间减少了疾病的严重程度.pdfVIP

Deletion of UCP2 in iNOS Deficient Mice Reduces the Severity of the Disease during Experimental Autoimmune Encephalomyelitis 1 1 2,3 4,5 1 Caroline Aheng , Nathalie Ly , Mairead Kelly , Saleh Ibrahim , Daniel Ricquier , Marie-Clotilde 1 6 Alves-Guerra *, Bruno Miroux * ´ ´ 1 Institut Cochin INSERM U1016, CNRS UMR8104, Faculte Paris Descartes, Paris, France, 2 Universite Paris-Descartes, site Necker, INSERMU845, Paris, France, 3 Laboratoire ˆ de Biochimie A, Hopital Necker-Enfants-Malades, Paris, France, 4 Genetics Group, Department of Dermatology, University of Luebeck, Luebeck, Germany, 5 Department of ´ Immunology, University of Rostock, Rostock, Germany, 6 Laboratoire de Biologie Physico-Chimique des Proteines Membranaires, Institut de Biologie Physico-Chimique, ´ CNRS UMR 7099, Universite Paris-Diderot, Paris, France Abstract Uncoupling protein 2 is a member of the mitochondrial anion carrier family that is widely expressed in neurons and the immune cells of humans. Deletion of Ucp2 gene in mice pre-activates the immune system leading to higher resistance toward infection and to an increased susceptibility to develop chronic inflammatory diseases as previously exemplified with the Experimental Autoimmune Encephalomyelitis (EAE), a mouse model for multiple sclerosis. Given that oxidative stress is enhanced in Ucp22/ 2 mice and that nitric oxide (NO) also plays a critical function in redox balance