Linked Life Data

8761305

Source:http://linkedlifedata.com/resource/pubmed/id/8761305

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-10-10
pubmed:abstractText
E1A oncogene expression increases the susceptibility of cells from several species to lysis by natural killer lymphocytes (NK cells). We asked whether this E1A-induced cellular phenotypic conversion is specific for NK cell recognition interactions with target cells or whether it results from an E1A effect that is mediated independently of recognition. E1A-positive and E1A-negative cell pairs were compared for cytolytic susceptibility to other types of killer cells that use recognition mechanisms different from those of NK cells. E1A-positive, NK-susceptible target cells were also preferentially lysed by cytotoxic T lymphocytes (CTL) that recognize only foreign MHC molecules, lymphokine-activated T cells that lack recognition specificity, and CTL whose conventional recognition mechanisms were bypassed by lectin treatment of target cells. E1A expression increased cellular susceptibility to both major mechanisms of killer cell lysis-perforin/granzyme lysis and Fas-dependent lysis. Furthermore, anti-Fas antibody lysed E1A-positive, but not E1A-negative, cells expressing comparable levels of cell surface Fas antigen. These results indicate that a major mechanism by which E1A induces cellular susceptibility to lysis involves a stage in the interaction of killer cells with their targets that follows and is independent of cell surface recognition.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
833-42
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
E1A oncogene expression in target cells induces cytolytic susceptibility at a post-recognition stage in the interaction with killer lymphocytes.
pubmed:affiliation
Robert W Lisle Research Laboratory in Immunology and Tumor Cell Biology, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't