Linked Life Data

10388794

Source:http://linkedlifedata.com/resource/pubmed/id/10388794

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-8-10
pubmed:abstractText
Previous studies have shown that activated T cells can successfully cross endothelial barriers and will accumulate in tissue which contains their specific antigen. Myelin specific T cells (e.g. myelin basic protein specific) are recognized to play an important role in the induction of experimental autoimmune demyelinating disease of the CNS and have been shown to induce blood-brain barrier breakdown effectively. In this study we injected T cells reactive to a non-neural antigen (ovalbumin) systemically into Lewis rats and caused them to accumulate in the thoracic dorsal column by a prior injection of ovalbumin. Selected rats were given systemic demyelinating antibody, antimyelin oligodendrocyte antibody (anti-MOG antibody), to provide evidence of permeability changes to the blood-brain barrier. These animals were compared with control rats given systemic anti-P0 monoclonal antibody and to other rats given a direct micro-injection (3 microliters) of anti-MOG antibody into the thoracic dorsal column. All animals were monitored by serial neurophysiological studies and by histological examination. Direct anti-MOG antibody injection produced a focal block in conduction at the injection site and a large circumscribed area of primary demyelination with axonal preservation within the dorsal column. An even more profound conduction block and more extensive plaque-like region of demyelination were seen in animals given antigen, activated T cells and systemic antibody. However, animals given antigen and T cells without relevant antibody did not show conduction impairment or demyelination, except when very large numbers of T cells were given; such rats developed severe irreversible axonal damage. This study demonstrates the blood-brain barrier is disrupted by activated T cells of non-neural specificity and allows large plaque-like regions of demyelination to form in the presence of circulating antimyelin antibody. The relevance of this finding to multiple sclerosis is discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-8950
pubmed:author
pubmed:issnType
Print
pubmed:volume
122 ( Pt 7)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1283-91
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10388794-Animals, pubmed-meshheading:10388794-Antibodies, pubmed-meshheading:10388794-Blood-Brain Barrier, pubmed-meshheading:10388794-Capillary Permeability, pubmed-meshheading:10388794-Dose-Response Relationship, Drug, pubmed-meshheading:10388794-Electrophysiology, pubmed-meshheading:10388794-Evoked Potentials, Somatosensory, pubmed-meshheading:10388794-Female, pubmed-meshheading:10388794-Injections, Spinal, pubmed-meshheading:10388794-Lymphocyte Activation, pubmed-meshheading:10388794-Myelin Proteins, pubmed-meshheading:10388794-Myelin Sheath, pubmed-meshheading:10388794-Myelin-Associated Glycoprotein, pubmed-meshheading:10388794-Nerve Block, pubmed-meshheading:10388794-Neural Conduction, pubmed-meshheading:10388794-Ovalbumin, pubmed-meshheading:10388794-Rats, pubmed-meshheading:10388794-Rats, Inbred Lew, pubmed-meshheading:10388794-Spinal Cord, pubmed-meshheading:10388794-T-Lymphocytes, pubmed-meshheading:10388794-Time Factors
pubmed:year
1999
pubmed:articleTitle
Activated non-neural specific T cells open the blood-brain barrier to circulating antibodies.
pubmed:affiliation
Institute of Clinical Neurosciences, The University of Sydney, Sydney, Australia Department of Neuroimmunology, Max Planck Institute for Psychiatry, Munich, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't