Linked Life Data

7900436

Source:http://linkedlifedata.com/resource/pubmed/id/7900436

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-4-27
pubmed:abstractText
In order to contribute to the prevention of malaria morbidity and mortality, especially in endemic zones, we have carried out a series of studies on cytokine interactions in an experimental model of cerebral malaria (CM). This rapidly lethal syndrome develops, in some strains of mice, upon infection with Plasmodium berghei ANKA (PbA). A crucial mediator of neurovascular lesions appears to be TNF, found in high amounts in relation with cerebral complications, in both experimental and human CM. In experimental CM, in vivo injections of anti-cytokine antibodies have been used to analyze the cascade of reactions leading to brain vascular damage. In this review, we fill focus on the interplay of cytokines responsible for TNF overproduction in experimental malaria, therefore delineating the subset of T cells whose activation can lead to pathology, and effector mechanisms of neurovascular lesions characteristic of mouse cerebral malaria, with recent findings that appear to involve an unexpected cell type, the blood platelet.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0303-8408
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
50-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Experimental cerebral malaria: possible new mechanisms in the TNF-induced microvascular pathology.
pubmed:affiliation
WHO-IRTC, Department of Pathology, Faculty of Medicine, University of Geneva.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't