Linked Life Data

2821117

Source:http://linkedlifedata.com/resource/pubmed/id/2821117

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1987-11-9
pubmed:abstractText
Glucocorticoids have been shown to play a major role in influencing the activation of B lymphocytes. In view of our recent observation that dexamethasone exerts a marked suppressive effect on an early event in B cell activation that is stimulated by anti-Ig antibody, we investigated its activity on other stimuli that induce intracellular events similar to those produced by anti-Ig antibody. Because the intracellular events that occur after B cell stimulation with phorbol myristate acetate and the calcium ionophore A23187 appear to mimic those that occur after B cell stimulation with anti-Ig antibody, we studied whether the cellular responses elicited by these activation stimuli are affected in a similar fashion by dexamethasone. Whereas anti-Ig antibody-stimulated entry of G0 B cells to the G1 and S phase of the cell cycle was markedly suppressed by dexamethasone, phorbol myristate acetate/A23187 stimulation of these events was resistant to dexamethasone. Our finding that anti-Ig-induced cross-linking of B cell surface Ig, as measured by surface Ig capping, was not inhibited by dexamethasone suggested that corticosteroids inhibit anti-Ig-induced B cell proliferation at a step distal to membrane Ig cross-linking and proximal to phosphatidylinositol bisphosphate hydrolysis. This hypothesis is supported by experiments presented in this manuscript which demonstrate that dexamethasone inhibits anti-Ig-stimulated phosphatidylinositol bisphosphate hydrolysis. We also found that dexamethasone markedly inhibited anti-Ig antibody-stimulated increases in intracellular ionized calcium concentrations. This dexamethasone-mediated suppression is time-dependent as it is not seen when B cells are cultured with dexamethasone for less than 6 hr. Our data suggest that the immunomodulatory activity of glucocorticoids is exerted by binding to its nuclear receptor, thereby preventing the generation of second messengers required for cell activation after agonist-receptor interaction.
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:day
15
pubmed:volume
139
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2516-23
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2821117-Animals, pubmed-meshheading:2821117-Antibodies, Anti-Idiotypic, pubmed-meshheading:2821117-Antigen-Antibody Reactions, pubmed-meshheading:2821117-B-Lymphocytes, pubmed-meshheading:2821117-Calcimycin, pubmed-meshheading:2821117-Calcium, pubmed-meshheading:2821117-Cell Cycle, pubmed-meshheading:2821117-Dexamethasone, pubmed-meshheading:2821117-Glucocorticoids, pubmed-meshheading:2821117-Inositol Phosphates, pubmed-meshheading:2821117-Killer Cells, Natural, pubmed-meshheading:2821117-Lymphocyte Activation, pubmed-meshheading:2821117-Mice, pubmed-meshheading:2821117-Phosphatidylinositols, pubmed-meshheading:2821117-Receptors, Antigen, B-Cell, pubmed-meshheading:2821117-Receptors, Glucocorticoid, pubmed-meshheading:2821117-T-Lymphocytes, pubmed-meshheading:2821117-Tetradecanoylphorbol Acetate
pubmed:year
1987
pubmed:articleTitle
Glucocorticoids suppress calcium mobilization and phospholipid hydrolysis in anti-Ig antibody-stimulated B cells.
pubmed:affiliation
Department of Medicine, Walter Reed Army Medical Center, Washington, DC 20014.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.