Linked Life Data

6976377

Source:http://linkedlifedata.com/resource/pubmed/id/6976377

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1982-3-13
pubmed:abstractText
Schistosoma mansoni granuloma modulation was first described in an in vivo murine model of schistosomiasis and was characterized as a diminished cellular responsiveness to newly formed eggs in chronic infections. This phenomenon of modulation was studied using an in vitro model of granuloma formation. Negative selection procedures using anti-Lyt-1.2, 2.2, and Qa-1 sera and complement on spleen cell populations from normal or S. mansoni-infected C57BL/6 or (C57BL/6 X A/J)F1 mice were examined for their effect on in vitro granuloma formation or modulation. These data suggest that there is a Lyt-1+2-, Qa-1+ T cell present in chronically infected spleen cells that is capable of inducing feedback suppression. In addition, selective removal of a population of Lyt-1-2+ T cells from chronically infected spleen cells augmented the ability of that population to form granulomas in vitro. The selective removal of Lyt-1+2- cells ablated the ability of chronically infected spleen cells to form in vitro granulomas. Granuloma formation is primarily dependent on a population of Lyt-1+, Qa-1+ cells, and modulation is dependent on 2 populations, 1 acting directly (Lyt-1-2+) and the other through a (Lyt-1+2-, Qa-1+) feedback mechanism of suppression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37-42
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
Delayed hypersensitivity granuloma formation and modulation around Schistosoma mansoni eggs in vitro. II. Regulatory T cell subsets.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't