Linked Life Data

18250416

Source:http://linkedlifedata.com/resource/pubmed/id/18250416

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-2-5
pubmed:abstractText
The high-affinity chain of the IL-7 receptor, IL-7Ralpha (CD127), is expressed by effector CD8 T cells that have the capacity to become memory cells. IL-7Ralpha expression is uniformly high on naive CD8 T cells, and the majority of these cells down-regulate expression upon antigenic challenge. At the peak of expansion, the fraction of effectors expressing high IL-7Ralpha varies depending on the response examined. The signals that a CD8 T cell receives during a response to Ag that lead to altered expression of IL-7Ralpha have not been fully defined. In vitro experiments demonstrated that Ag alone is sufficient to down-regulate IL-7Ralpha on all cells and most of the cells rapidly re-express the receptor upon removal from Ag. Expression was not altered by the B7.1 costimulatory ligand or when IL-12 was present to provide the signal needed for development of effector functions, indicating that TCR engagement is sufficient to regulate IL-7Ralpha expression. Consistent with this, in vivo priming with peptide Ag resulted in IL-7Ralpha expression that inversely correlated with Ag levels, and expression levels were not changed when IL-12 or adjuvant were administered with Ag. A large fraction of the cells present at the peak of expansion had re-expressed IL-7Ralpha, but most of these cells failed to survive; those that did survive expressed high IL-7Ralpha levels. Thus, Ag-dependent signals regulate IL-7Ralpha levels on responding CD8 T cells, and this occurs whether the responding cells become fully activated or are rendered tolerant by administration of peptide Ag alone.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
180
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2107-16
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:18250416-Animals, pubmed-meshheading:18250416-Antigens, pubmed-meshheading:18250416-CD8-Positive T-Lymphocytes, pubmed-meshheading:18250416-Cells, Cultured, pubmed-meshheading:18250416-Clone Cells, pubmed-meshheading:18250416-Down-Regulation, pubmed-meshheading:18250416-Egg Proteins, pubmed-meshheading:18250416-G0 Phase, pubmed-meshheading:18250416-Immune Tolerance, pubmed-meshheading:18250416-Immunologic Memory, pubmed-meshheading:18250416-Listeria monocytogenes, pubmed-meshheading:18250416-Lymphocyte Activation, pubmed-meshheading:18250416-Mice, pubmed-meshheading:18250416-Mice, Congenic, pubmed-meshheading:18250416-Mice, Inbred C57BL, pubmed-meshheading:18250416-Mice, Transgenic, pubmed-meshheading:18250416-Ovalbumin, pubmed-meshheading:18250416-Peptide Fragments, pubmed-meshheading:18250416-Receptors, Interleukin-7, pubmed-meshheading:18250416-Reproducibility of Results
pubmed:year
2008
pubmed:articleTitle
Antigen controls IL-7R alpha expression levels on CD8 T cells during full activation or tolerance induction.
pubmed:affiliation
Center for Immunology, Department of Laboratory Medicine and Pathology, University of Minnesota, 420 Delaware Street Southeast, Minneapolis, MN 55455, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural