The Proteolipid Protein and its Possible Role in the Pathology of Multiple Sclerosis
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Authors
Latham, Amy E.
Issue Date
1999
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
Multiple sclerosis is a neurological disorder wherein myelin in the central nervous
system (CNS) is destroyed through a chronic inflammatory process. The cause of the
inflammation is not known, but is believed to be a result of an autoimmune process in
which autoreactive T lymphocytes attack the myelin. Oligodendroglia, the cells which
supply myelin in the CNS, are largely comprised of the proteolipid protein (PLP).
Relatively little is known about PLP because it is difficult to work with due to its high
hydrophobicity, but new techniques using fusion constructs have elucidated its
importance to cells. In this experiment, a series of mammalian expression vectors that
used either the CMV (constitutive mammalian) promoter or a bacterial tetracycline
regulated promoter called the PLP Tet-On promoter were created to examine the
processing of normal and mutant PLP proteins. Results indicate that in the 293 human
embryonic kidney cell, PLP is regulated beyond the translational level by the
ubiquitinlproteasome system. Current theory claims that the peptides resulting from PLP
proteasome degradation are recognized as antigenic by the immune system and that
oligodendrocytes displaying these peptides are targeted for cell death by autoreactive T
lymphocytes. This knowledge provides important information about the activities ofPLP
in the cell and may help demonstrate that PLP is the principle protein involved in the
oligodendrocyte death that leads to the pathology of multiple sclerosis.
Description
v, 28 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.