Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (119)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by ZAJICEK, J. P.
Right arrow Articles by COMPSTON, D. A. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by ZAJICEK, J. P.
Right arrow Articles by COMPSTON, D. A. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Brain, Vol. 115, No. 6, 1611-1631, 1992
© 1992 Guarantors of Brain

research-article

INTERACTIONS BETWEEN OLIGODENDROCYTES AND MICROGLIA

A MAJOR ROLE FOR COMPLEMENT AND TUMOUR NECROSIS FACTOR IN OLIGODENDROCYTE ADHERENCE AND KILLING

J. P. ZAJICEK1, M. WING2, N. J. SCOLDING1 and D. A. S. COMPSTON1

1University of Cambridge Neurology unit Cambridge, UK 2Molecular Immunopathology Unit, MRC Centre Addenbrookes Hospital Cambridge, UK

Correspondence to: Correspondence to: J. P. Zajicek, University of Cambridge Neurology unit, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK.

Interactions between rat microglia and oligodendrocytes were examined in vitro in order to characterize the stages of adherence, phagocytosis and cytotoxicity against oligodendrocytes by microglia. Under resting conditions, microglia showed minimal contact with oligodendrocytes and exhibited surface staining of myelin basic protein and myelin debris only; they were not cytotoxic for oligodendrocytes and did not produce tumour necrosis factor (TNF). On activation with either {Gamma}-interferon or lipopolysaccharide and interferon, these cells increased surface binding for myelin basic protein, showed greater contact with living oligodendrocytes and produced TNF in both secreted and cell surface bound forms. Secreted TNF was capable of killing oligodendrocytes but the cell surface bound form did this more efficiently. In the presence of complement, activated microglia showed significant phagocytosis of myelin basic protein which was not obvious in the unactivated cells. These results suggest that activated microglia in the presence of complement are sufficient to kill and phagocytose the oligodendrocyte-myelin complex in vitro

Received April 13, 1992. Revised June 8, 1992. Accepted June 16, 1992.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mult SclerHome page
M H Barnett, A P. Henderson, and J W Prineas
The macrophage in MS: just a scavenger after all? Pathology and pathogenesis of the acute MS lesion
Multiple Sclerosis, April 1, 2006; 12(2): 121 - 132.
[Abstract] [PDF]

Home page
 BrainHome page
A. Jurewicz, M. Matysiak, K. Tybor, L. Kilianek, C. S. Raine, and K. Selmaj
Tumour necrosis factor-induced death of adult human oligodendrocytes is mediated by apoptosis inducing factor
Brain, November 1, 2005; 128(11): 2675 - 2688.
[Abstract] [Full Text] [PDF]

Home page
 Postgrad. Med. J.Home page
J Zajicek
Diagnosis and disease modifying treatments in multiple sclerosis
Postgrad. Med. J., September 1, 2005; 81(959): 556 - 561.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
D. C. Shields, K. E. Schaecher, T. C. Saido, and N. L. Banik
A putative mechanism of demyelination in multiple sclerosis by a proteolytic enzyme, calpain
PNAS, September 28, 1999; 96(20): 11486 - 11491.
[Abstract] [Full Text] [PDF]

Home page
 PediatricsHome page
O. Dammann and A. Leviton
Brain Damage in Preterm Newborns: Might Enhancement of Developmentally Regulated Endogenous Protection Open a Door for Prevention?
Pediatrics, September 1, 1999; 104(3): 541 - 550.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
P. G. Sullivan, A. J. Bruce-Keller, A. G. Rabchevsky, S. Christakos, D. K. St. Clair, M. P. Mattson, and S. W. Scheff
Exacerbation of Damage and Altered NF-kappa B Activation in Mice Lacking Tumor Necrosis Factor Receptors after Traumatic Brain Injury
J. Neurosci., August 1, 1999; 19(15): 6248 - 6256.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
K. Akassoglou, J. Bauer, G. Kassiotis, M. Pasparakis, H. Lassmann, G. Kollias, and L. Probert
Oligodendrocyte Apoptosis and Primary Demyelination Induced by Local TNF/p55TNF Receptor Signaling in the Central Nervous System of Transgenic Mice : Models for Multiple Sclerosis with Primary Oligodendrogliopathy
Am. J. Pathol., September 1, 1998; 153(3): 801 - 813.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
S. D. D'Souza, B. Bonetti, V. Balasingam, N. R. Cashman, P. A. Barker, A. B. Troutt, C. S. Raine, and J. P. Antel
Multiple Sclerosis: Fas Signaling in Oligodendrocyte Cell Death
J. Exp. Med., December 1, 1996; 184(6): 2361 - 2370.
[Abstract] [Full Text] [PDF]

Home page
 Mult SclerHome page
J Zajicek and A Compston
Mechanisms of damage and repair in multiple sclerosis -- a review
Multiple Sclerosis, June 1, 1995; 1(2): 61 - 72.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.