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Spontaneous CNS remyelination in beta(2) microglobulin-deficient mice following virus-induced demyelination
Author(s): Miller DJ, RiveraQuinones C, Njenga MK, Leibowitz J, Rodriguez M
Source: JOURNAL OF NEUROSCIENCE    Volume: 15    Issue: 12    Pages: 8345-8352    Published: DEC 1995  
Times Cited: 31     References: 44     
Abstract: Animal models with selective genetic immunodeficiencies are useful tools to identify pathogenic mechanisms of disease. Resistant (C57BL/6F 129/5) (H-2(b)) mice are rendered susceptible to Theiler's murine encephalomyelitis virus-induced demyelination by genetic disruption of the beta(2) microglobulin gene [beta(2)m(-/-)]. The absence of beta(2)m prevents the expression of major histocompatibility complex class I molecules and normal levels of functional CD8(+) T cells. We tested whether genetic depletion of beta(2)m would permit CNS remyelination after chronic demyelination induced by the Daniel's strain of Theiler's virus. In contrast to the minimal spontaneous remyelination observed in SJL/J mice after infection with the Daniel's strain of Theiler's virus, chronically infected beta(2)m(-/-) mice showed extensive and progressive spontaneous CNS remyelination at 6, 12, and 18 months after infection. Spontaneous remyelination by both oligodendrocytes and Schwann cells occurred despite the presence of persistent virus antigen and RNA, but was associated with diminished virus-specific humoral and delayed-type hypersensitivity responses. These experiments support the hypothesis that the immune response inhibits myelin regeneration after virus-induced CNS demyelination.
Document Type: Article
Language: English
Addresses:
1. MAYO CLIN & MAYO FDN, DEPT IMMUNOL, ROCHESTER, MN 55905 USA
2. MAYO CLIN & MAYO FDN, DEPT NEUROL, ROCHESTER, MN 55905 USA
3. UNIV TEXAS, SCH MED, DEPT PATHOL & LAB MED, HOUSTON, TX 77225 USA
Publisher: OXFORD UNIV PRESS INC, JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513
Subject Category: Neurosciences
IDS Number: TP154
ISSN: 0270-6474
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