Genetic models for CNS inflammation.
The use of transgenic technology to over-express or prevent expression of genes encoding molecules related to inflammation has allowed direct examination of their role in experimental disease. This article reviews transgenic and knockout models of CNS demyelinating disease, focusing primarily on the autoimmune disease multiple sclerosis, as well as conditions in which an inflammatory response makes a secondary contribution to tissue injury or repair, such as neurodegeneration, ischemia and trauma.
Owens
T
T
Neuroimmunology Unit, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. trevor@med.mcgill.ca
Wekerle
H
H
Antel
J
J
D000818:Animals; D002490:Central Nervous System / Q000276:immunology*; D018925:Chemokines / Q000276:immunology; D002986:Clinical Trials as Topic; D016207:Cytokines / Q000276:immunology; D003711:Demyelinating Diseases / Q000235:genetics* / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D008957:Models, Genetic; D009103:Multiple Sclerosis / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D018925:Chemokines; D016207:Cytokines; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma