DYSMYELINATION IN CLASS-I MHC TRANSGENIC MICE

Turnley, AM; Morahan, G

Author(s): Turnley, AM; Morahan, G;
Details: Publication Year 1995-11-01,Volume 32,Issue #4,Page 286-294
Journal Title: MICROSCOPY RESEARCH AND TECHNIQUE
Publication Type: Journal Article
Abstract: Why is it that oligodendrocytes do not normally express major histocompatibility complex (MHC) molecules? To examine the effect of aberrant MHC expression in oligodendrocytes, transgenic mice have been produced which expressed the class I MHC gene, H-2K(b), under direction of the MBP promoter [Turnley et al. (1991b) Nature, 353:566-569; Yoshioka et al. (1991) Mol. Cell. Biol., 11:5479-5486]. A proportion of these mice exhibited a shivering phenotype, with tonic seizures and early death. Oligodendrocyte function and viability was shown to be affected, resulting in severe dysmyelination of the CNS. Is this phenomenon of cell damage due to aberrant expression of MHC molecules restricted to oligodendrocytes, and could other, non-MHC molecules, when aberrantly expressed, result in similar cell damage? This paper discusses these questions and examines possible mechanisms for the oligodendrocyte damage and hypomyelination observed in these transgenic mice. Finally, the implications of aberrant MHC expression in oligodendrocytes for demyelinating diseases such as multiple sclerosis are discussed. (C) 1995 Wiley-Liss, Inc.
Publisher: WILEY-LISS
Keywords: MAJOR HISTOCOMPATIBILITY COMPLEX; TUMOR NECROSIS FACTOR; MYELIN BASIC-PROTEIN; CENTRAL-NERVOUS-SYSTEM; PANCREATIC BETA-CELLS; MESSENGER-RNA LEVELS; MULTIPLE-SCLEROSIS; INTERFERON-GAMMA; SURFACE EXPRESSION; SCHWANN-CELLS
Publisher's Version: https://doi.org/10.1002/jemt.1070320403
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 1995-11-01 12:00:00