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Major histocompatibility complex Class I expression in oligodendrocytes induces hypomyelination in transgenic mice
Author(s) -
Power C.,
Kong P.A.,
Trapp B.D.
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19960415)44:2<165::aid-jnr9>3.0.co;2-b
Subject(s) - myelin , myelin basic protein , remyelination , oligodendrocyte , major histocompatibility complex , biology , proteolipid protein 1 , genetically modified mouse , transgene , microglia , mhc class i , immunology , central nervous system , mhc class ii , multiple sclerosis , neuroscience , microbiology and biotechnology , antigen , gene , genetics , inflammation
Increased expression of MHC Class I occurs in the central nervous system in association with demyelinating diseases such as multiple sclerosis and experimental allergic encephalomyelitis. To determine if MHC Class I expression by oligodendrocytes induces white matter pathology, the MHC Class I gene was expressed in transgenic mice under the control of the myelin basic protein (MBP) promoter. These mice display a neurological phenotype at 21 days‐of‐age. We examined these mice at 1, 3, and 12 weeks‐of‐age. MHC Class I was detected in the brains and spinal cords of transgenic mice but not in control mice. Class I was located in oligodendrocyte perikarya but not in myelin sheaths. The central nervous system of these transgenic mice was hypomyelinated and contained hypertrophic microglia and astrocytes. These observations establish that Class I expression by oligodendrocytes delays normal myelination but does not cause inflammatory demyelination. This hypomyelinating animal model is of potential use in studying the interactions between immunologically active molecules and remyelination in disorders of myelin. © 1996 Wiley‐Liss, Inc.