Linked Life Data

1486453

Source:http://linkedlifedata.com/resource/pubmed/id/1486453

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1993-2-24
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-8950
pubmed:author
pubmed:issnType
Print
pubmed:volume
115 ( Pt 6)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1611-31
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Interactions between oligodendrocytes and microglia. A major role for complement and tumour necrosis factor in oligodendrocyte adherence and killing.
pubmed:affiliation
University of Cambridge Neurology Unit, Addenbrookes Hospital, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't