Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-6-12
pubmed:abstractText
CD8+ T cells are known to play a major role in regulating immune functions under normal and disease conditions. In this study a radioligand binding assay was used to quantitate histamine type II (H2) receptors on activated T cells. The objective was to examine the expression of H2 receptors on T cells during activation with interleukin-2 (IL-2) and treatment with cimetidine. Activated suppressor T cells induced by concanavalin A+IL-2 showed a significant (p less than 0.01) increase in H2 receptors compared to the control nonactivated T cells. The T cells expressing the H2 receptors were identified as CD8+ cells; those among them that had an enhanced level of H2 receptors were identified as CD25+. Treatment of activated suppressor cells with the H2 receptor antagonist cimetidine at a concentration of 10(-5) M significantly reduced the number of H2 receptors. Suppressor cells induced by Con A+IL-2 were able to suppress both IgG and IgM production that was reversible with cimetidine. Incubation of lymphocytes with 50 U/ml IL-2 alone in 3-day culture significantly (p less than 0.005) enhanced H2 receptor expression. These studies demonstrate that activated suppressor T cells that are CD8+CD25+ have enhanced levels of H2 receptors and can be modulated by cimetidine.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1018-2438
pubmed:author
pubmed:issnType
Print
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8-16
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Modulation of histamine type II receptors on CD8+ T cells by interleukin-2 and cimetidine.
pubmed:affiliation
John Wayne Institute for Cancer Treatment and Research, Santa Monica, CA 90404.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't