Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination.
Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.
van Engelen
B G
BG
Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA.
Pavelko
K D
KD
Rodriguez
M
M
D000818:Animals; D002490:Central Nervous System / Q000276:immunology / Q000503:physiopathology*; D003711:Demyelinating Diseases / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D008244:Lysophosphatidylcholines / Q000633:toxicity; D051379:Mice; D009186:Myelin Sheath / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D009416:Nerve Regeneration; D011051:Poliomyelitis / Q000503:physiopathology; D017945:Theilovirus
D007074:Immunoglobulin G; D016756:Immunoglobulins, Intravenous; D008244:Lysophosphatidylcholines