Linked Life Data

6956630

Source:http://linkedlifedata.com/resource/pubmed/id/6956630

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1982-12-3
pubmed:abstractText
Resident peritoneal M phi of C3H/HeN mice co-cultured with splenic lymphocytes suppressed proliferation to mitogens. This M phi-mediated suppression was significantly reduced by in vitro treatment of M phi with fibroblast interferon (IFN-beta). Conversely, M phi-mediated natural tumor cytolysis was augmented by M phi treatment with IFN-beta. Depletion of Ia-bearing (Ia+) M phi by means of anti-Ia serum and C treatment did not affect M phi-mediated suppression or M phi-mediated natural cytotoxicity. This suggested that Ia-negative (Ia-) M phi were responsible for the effector phase of these two M phi functions. The IFN-beta-induced increase in M phi cytolysis was not affected by depletion of Ia+ cells; however, modulation of suppressive activity by IFN-beta was found to be highly dependent on the presence of Ia+ M phi. This observation indicated that different M phi subpopulations were involved in the regulation of suppressive and tumoricidal activity. The results indicating different regulatory M phi were supported by experiments with C3H/HeJ mice. C3H/HeJ M phi do not develop high cytolytic activity in response to a variety of stimuli; however, M phi from C3H/HeJ mice were able to exert suppressive activity, which was reduced by treatment with IFN-beta.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
129
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1854-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Regulation of macrophage suppression and cytotoxicity by interferon role of Ia-bearing macrophages.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't