Glial expression of tumor necrosis factor in transgenic animals: how do these models reflect the "normal situation"?
Recent progress in the field of experimental genetics, which enables the selective and conditional ablation or dysregulation in the expression of specific genes in mice, and its application to the study of experimentally inducible models for human disease, have contributed enormously to our understanding of the molecules and mechanisms that underlie autoimmunity and inflammation in the CNS. This article describes the lessons learned from the application of such technology to the study of the tumor necrosis factor-alpha (TNF) ligand/receptor system in the CNS. Important roles for TNF and its two membrane-bound receptors in the initiation and support of CNS inflammation, the development of CNS autoimmunity, and possibly in the resolution of T-cell-mediated disease, as well as their implications for our understanding of the "normal" cellular and molecular mechanisms that underlie CNS pathology, are discussed.
Probert
L
L
Laboratory of Molecular Genetics, Hellenic Pasteur Institute, Athens, Greece. lesley_probert@hol.gr
Akassoglou
K
K
D000818:Animals; D030801:Animals, Genetically Modified / Q000276:immunology*; D002490:Central Nervous System / Q000276:immunology*; D004195:Disease Models, Animal; D004660:Encephalitis / Q000276:immunology*; D006801:Humans; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology; D009457:Neuroglia / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology* / Q000502:physiology
D014409:Tumor Necrosis Factor-alpha