Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-3-5
pubmed:abstractText
Experimental autoimmune encephalomyelitis (EAE) is an inflammatory autoimmune disease of the central nervous system that serves as a model for the human disease multiple sclerosis. Paralysis is "induced" by CD4+ T cells of the Th1 phenotype. Tumor necrosis factor (TNF), a Th1 type cytokine, has been shown to be upregulated in the CNS during the onset of EAE, and systemic manipulations of TNF have had substantial effects on disease progression. However, the precise role of TNF in EAE has been called into question by recent experiments utilizing TNF and lymphotoxin knockout mice. We demonstrate here that the local delivery of TNF by myelin basic protein (MBP)-specific T cells, retrovirally transduced to express TNF, exacerbated MBP-induced disease following adoptive transfer into syngeneic mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1521-6616
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
10-4
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Local delivery of TNF by retrovirus-transduced T lymphocytes exacerbates experimental autoimmune encephalomyelitis.
pubmed:affiliation
Department of Medicine, Stanford University School of Medicine, Stanford, California, 94305-5111, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.