Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1985-10-16
pubmed:abstractText
Recombinant-derived interferon-gamma (reIFN-gamma) was found to inhibit B cell proliferation that was stimulated by soluble goat anti-mouse IgD or goat anti-mouse IgM antibodies, but not that stimulated by Sepharose-bound anti-Ig antibodies. Recombinant IFN-gamma also inhibited the BSF-1-enhanced soluble anti-Ig B cell proliferation but did not block BSF-1 enhancement of Sepharose anti-Ig-stimulated B cell DNA synthesis. Recombinant IFN-gamma concentrations as low as 0.001 U/ml were effective in suppressing the soluble anti-Ig-stimulated B cell proliferative response, and this inhibitory effect could be partially reversed by co-culture with a hybridoma anti-IFN-gamma antibody. Recombinant IFN-gamma appeared not to inhibit action of resting B cells from G0 to early G1, because it did not inhibit the increases in cell size that were stimulated by anti-delta antibody. However, it was effective in partially suppressing the anti-delta-induced increases in expression of B cell surface Ia. For reIFN-gamma to exert its maximum suppressive effect, it had to be added within the first 7 hr after the onset of culture with anti-Ig. Because reIFN-gamma is a lymphokine that can be detected in vivo, we suggest that it may play a key role in influencing physiologic B cell activation that is induced by antigens or immune complex-mediated cross-linking of surface Ig.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
135
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2513-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
Recombinant interferon-gamma inhibits the B cell proliferative response stimulated by soluble but not by Sepharose-bound anti-immunoglobulin antibody.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.