Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-8-31
pubmed:abstractText
The inhibition of mitogen induced differentiation by antibodies directed against cell surface immunoglobulins has been used as a polyclonal model system for the study of immune complex mediated down-regulation of the B cell response. The mechanism of this inhibition may also be similar to the ability of gamma globulins coupled to haptens to induce hapten specific B cell tolerance. By biosynthetic labeling of newly synthesized mRNA and of polypeptide chains, the molecular level of inhibition of lipopolysaccharide (LPS) induced B cell differentiation by whole anti-immunoglobulins (anti-Ig) has been examined. It was found that neither blast transformation nor initiation of DNA synthesis is prevented. However, the specific enhancement of transcription of the mu and kappa chain genes induced by LPS is inhibited resulting in the total abrogation of the increase in steady state level of mu s mRNA. In contrast, the basal level of transcription necessary for maintenance of the synthesis of mRNA for membrane IgM and IgD is not affected. Accordingly, it is the specific inhibition of enhanced initiation of RNA polymerases at the mu-delta gene complex which results in the previously documented decrease in IgM secretion. Moreover, since there is also no detectable C gamma transcription in cells stimulated with LPS in the presence of anti-Ig, the further differentiation of IgG secretion in LPS stimulated cells is also prevented.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0724-6803
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Molecular basis for the inhibition of LPS induced differentiation by anti-immunoglobulin.
pubmed:affiliation
Department of Pathology, University of Texas Health Science Center, Dallas 75235.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.