Induction of anti-myelin antibodies in EAE and their possible role in demyelination.

Loading...
Thumbnail Image

Date

1991-12

Journal Title

Journal ISSN

Volume Title

Repository Usage Stats

167
views
239
downloads

Citation Stats

Abstract

Experimental allergic encephalomyelitis is characterized by invasion of lymphocytes and macrophages into the central nervous system resulting in inflammation, edema, and demyelination. Sera from Lewis rats from 7-95 days after immunization with purified guinea pig CNS myelin were examined with respect to their ability to opsonize myelin. This was correlated with the appearance of antibody components and the relative amounts of antibody to myelin basic protein (MBP) and proteolipid protein (PLP). Sera from rats 10-95 days after immunization preincubated with purified myelin induced phagocytosis of myelin by cultured macrophages with the resulting production of cholesterol ester. This opsonization activity as measured by the percentage of cholesterol esterified reached a peak at 26-27 days after immunization but remained significantly elevated up to 95 days post-immunization compared to the activity of serum from the Freund's adjuvant-injected controls. Immunoblots of the sera revealed a gradual increase in antibody activity against myelin components. ELISA assays for MBP and PLP antibody showed a similar pattern. Antibody to galactocerebroside (GC) was not detected by immunostains nor by the ELISA assay. Areas of demyelination were observed histologically by luxol-fast blue stained spinal cords up to 60 days post-immunization. These results indicate that antibodies to myelin protein when given access to myelin through or within the blood brain barrier could initiate or enhance the phagocytic response by peripheral or resident macrophages.

Department

Description

Provenance

Citation

Published Version (Please cite this version)

10.1002/jnr.490300404

Publication Info

Sadler, RH, MA Sommer, LS Forno and ME Smith (1991). Induction of anti-myelin antibodies in EAE and their possible role in demyelination. J Neurosci Res, 30(4). pp. 616–624. 10.1002/jnr.490300404 Retrieved from https://hdl.handle.net/10161/11767.

This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.

Scholars@Duke

Sommer

Marc A. Sommer

Professor of Biomedical Engineering

We study circuits for cognition. Using a combination of neurophysiology and biomedical engineering, we focus on the interaction between brain areas during visual perception, decision-making, and motor planning. Specific projects include the role of frontal cortex in metacognition, the role of cerebellar-frontal circuits in action timing, the neural basis of "good enough" decision-making (satisficing), and the neural mechanisms of transcranial magnetic stimulation (TMS).


Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.