Linked Life Data

2666570

Source:http://linkedlifedata.com/resource/pubmed/id/2666570

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-8-31
pubmed:abstractText
With virus-infected autologous and allogenic mononuclear cells as specific targets, the development of cell-mediated cytotoxic reactivity to respiratory syncytial virus (RSV) was studied in peripheral blood lymphocytes (PBL) in groups of infants with acute RSV infection and in other control groups of subjects during a community outbreak of RSV infection. No RSV-specific cellular cytotoxicity was observed in cord blood lymphocytes and in other uninfected controls. The PBL of infants with acute RSV infection exhibited significant cellular cytotoxic response. The activity peaked early, usually within 1 week after infection. The response appeared to be age-dependent. Over 65% of infants 6-24 months of age and about 35-38% of infants under 5 months of age exhibited cellular cytotoxicity to RSV. Cellular cytotoxic reactivity was observed against autologous and less frequently against allogenic RSV-infected target cells. These findings suggest the appearance of virus-specific cell-mediated cytotoxic immune response after acute RSV infection. The development of cellular cytotoxic responses may play a role in the mechanisms of protection against or the pathogenesis of RSV infection in man.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0146-6615
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Development of cell-mediated cytotoxic immunity to respiratory syncytial virus in human infants following naturally acquired infection.
pubmed:affiliation
Department of Pediatrics, Sapporo Medical College, Japan.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.