Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1983-4-7
pubmed:abstractText
We have attempted to determine what host mechanisms are responsible for inducing a rapid decrease in the number of Friend leukemia cells (FLC) in the peritoneal cavity of interferon-treated mice. By injecting radiolabelled FLC, we showed that there was a greater loss of radioactivity from individual interferon-treated mice than from control mice. Thus, it was likely that fewer cells were recovered from the peritoneal cavity of interferon-treated mice because of cell destruction. Treatment of mice with interferon limited to the period preceding tumor-cell inoculation conferred some degree of antitumor activity, although this regimen was far less effective than when interferon treatment was initiated and continued daily after tumor-cell inoculation. We have been unable to transfer any antitumor activity with peritoneal washings containing macrophages and lymphocytes from interferon-treated donor mice to tumor-inoculated recipient mice. Inoculation of silica particles i.p., which destroys macrophage function and may affect NK cell activity, did not abrogate interferon's antitumor activity. We suggest that interferon induces a host-mediated antitumor effect by mechanisms which are not mediated by easily recoverable soluble factors or by cytotoxic cells. The nature of this potent interferon-induced host mechanism remains unknown.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
821-5
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Antitumor effects of interferon in mice injected with interferon-sensitive and interferon-resistant Friend leukemia cells. II. Role of host mechanisms.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't