Linked Life Data

2900149

Source:http://linkedlifedata.com/resource/pubmed/id/2900149

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1988-9-9
pubmed:abstractText
The membrane CD2 molecule appears to play an important role in T cell activation. Indeed, T cell stimulation by some combinations of anti-CD2 monoclonal antibodies (mAb) can result in antigen-independent expression of helper function as assessed by proliferation and lymphokine secretion. We report here that T cell stimulation by a combination of two anti-CD2 mAb recognizing GT2 and T11(1) epitopes, respectively, cannot alone induce T helper clones to proliferate when preincubated in culture medium devoid of exogenous interleukin 2 (IL2). The concerted action of both anti-GT2 + T11(1) mAb and exogenous recombinant IL2 is required to induce cloned helper T cells to produce IL 2 and interferon-gamma to significantly increase IL2 receptors (IL2R) and finally to divide by an autocrine mechanism, whereas each signal alone has no effect. This therefore suggests that, under some conditions of CD2 stimulation, two minimal signals may be delivered through CD2 and IL2R and act synergistically to achieve a complete expression of T helper cell functions. Moreover, analysis of phosphatidylinositol and phosphatidic acid metabolic changes mediated by each signal separately or together suggests that, in this model, IL2 increases the phosphoinositide turnover induced by anti-CD2 antibodies up to a level required for helper function acquisition.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1123-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Activation signals via CD2 molecule and interleukin 2 receptor act in synergy for helper function induction.
pubmed:affiliation
INSERM U 152, Hôpital Cochin, Paris, France.
pubmed:publicationType
Journal Article