Linked Life Data

1891717

Source:http://linkedlifedata.com/resource/pubmed/id/1891717

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5025
pubmed:dateCreated
1991-10-17
pubmed:abstractText
Viruses frequently persist in neurons, suggesting that these cells can evade immune surveillance. In a mouse model, 5 x 10(6) cytotoxic T lymphocytes (CTLs), specific for lymphocytic choriomeningitis virus (LCMV), did not lyse infected neurons or cause immunopathologic injury. In contrast, intracerebral injection of less than 10(3) CTL caused disease and death when viral antigens were expressed on leptomeningeal and choroid plexus cells of the nervous system. The neuronal cell line OBL21 expresses little or no major histocompatibility (MHC) class I surface glycoproteins and when infected with LCMV, resisted lysis by virus-specific CTLs. Expression of MHC heavy chain messenger RNA was limited, but beta 2-microglobulin messenger RNA and protein was made normally. OBL21 cells were made sensitive to CTL lysis by transfection with a fusion gene encoding another MHC class I molecule. Hence, neuronal cells probably evade immune surveillance by failing to express MHC class I molecules.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
253
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1283-5
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Viral persistence in neurons explained by lack of major histocompatibility class I expression.
pubmed:affiliation
Department of Neuropharmacology, Scripps Clinic and Research Foundation, La Jolla, CA 92037.
pubmed:publicationType
Journal Article