Linked Life Data

14707103

Source:http://linkedlifedata.com/resource/pubmed/id/14707103

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-1-6
pubmed:abstractText
An inappropriate cross talk between activated T lymphocytes infiltrating the CNS and neural cells can sustain the onset and progression of demyelination and axonal degeneration in neuroinflammatory diseases. To mimic this deleterious cross talk, we designed an experimental paradigm consisting of transient cocultures of T lymphocytes chronically activated by retrovirus infection (not virus productive) with human multipotent neural precursors or primary oligodendrocytes from rat brain. We showed that activated T lymphocytes induced apoptotic death of multipotent neural progenitors and immature oligodendrocytes after a progressive collapse of their process extensions. These effects were reminiscent of those induced by brain semaphorin on neural cells. Blockade by specific Abs of soluble CD100 (sCD100)/semaphorin 4D released by activated T cells, or treatment with rsCD100, demonstrated that this immune semaphorin has the ability to collapse oligodendrocyte process extensions and to trigger neural cell apoptosis, most likely through receptors of the plexin family. The specific presence of sCD100 in the cerebrospinal fluid and of CD100-expressing T lymphocytes in the spinal cord of patients suffering with neuroinflammatory demyelination pointed to the potential pathological effect of sCD100 in the CNS. Thus, our results show that CD100 is a new important element in the deleterious T cell-neural cell cross talk during neuroinflammation and suggest its role in demyelination or absence of remyelination in neuroinflammatory diseases including multiple sclerosis and human T lymphotropic virus type 1-associated myelopathy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
172
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1246-55
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14707103-Adult, pubmed-meshheading:14707103-Aged, pubmed-meshheading:14707103-Animals, pubmed-meshheading:14707103-Antigens, CD, pubmed-meshheading:14707103-Apoptosis, pubmed-meshheading:14707103-Cell Communication, pubmed-meshheading:14707103-Cell Differentiation, pubmed-meshheading:14707103-Cells, Cultured, pubmed-meshheading:14707103-Coculture Techniques, pubmed-meshheading:14707103-Female, pubmed-meshheading:14707103-Humans, pubmed-meshheading:14707103-Jurkat Cells, pubmed-meshheading:14707103-Lymphocyte Activation, pubmed-meshheading:14707103-Male, pubmed-meshheading:14707103-Membrane Glycoproteins, pubmed-meshheading:14707103-Middle Aged, pubmed-meshheading:14707103-Nerve Tissue Proteins, pubmed-meshheading:14707103-Neurons, pubmed-meshheading:14707103-Oligodendroglia, pubmed-meshheading:14707103-Paraparesis, Tropical Spastic, pubmed-meshheading:14707103-Rats, pubmed-meshheading:14707103-Receptors, Cell Surface, pubmed-meshheading:14707103-Semaphorins, pubmed-meshheading:14707103-Solubility, pubmed-meshheading:14707103-Stem Cells, pubmed-meshheading:14707103-T-Lymphocyte Subsets
pubmed:year
2004
pubmed:articleTitle
Semaphorin CD100 from activated T lymphocytes induces process extension collapse in oligodendrocytes and death of immature neural cells.
pubmed:affiliation
INSERM Unit 433, Experimental Neurobiology and Physiopathology, Federative Institut of Neuroscience 19, Faculty of Medicine R Laennec, rue G. Paradin, 69372 Lyon CEDEX 08, France. giraudon@lyon.inserm.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't