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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
1987-3-24
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pubmed:abstractText |
Cell surface expression of CD4, an invariant membrane glycoprotein, is characteristic of the MHC class II-restricted T cell helper/inducer subset. Although the specificity and restriction patterns of T lymphocytes are determined by the T cell receptor for antigen, CD4 might represent an additional "interaction" molecule that is required to strengthen the interaction between T cells, antigen, and antigen-presenting cells. In this manuscript, we have shown that the cell surface expression of CD4 is correlated with activation of T cells. Data presented in this paper have demonstrated, for the first time, that antigenic stimulation of human T cell clones caused a decrease in the expression of the CD4 marker (as well as to the CD3 marker) to about 50% of the constitutive level. As previously demonstrated, PMA caused modulation of CD4 and CD3, which suggested that phosphorylation by protein kinase C played a crucial role in the regulation of the expression of both markers. The parallel down-regulation of CD3 and CD4 after antigen stimulation suggested that both markers might be members of a multimolecular complex mediating T cell activation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
|
pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
138
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1351-4
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:3100638-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:3100638-Antigens, Surface,
pubmed-meshheading:3100638-Cell Differentiation,
pubmed-meshheading:3100638-Endocytosis,
pubmed-meshheading:3100638-Humans,
pubmed-meshheading:3100638-Lymphocyte Activation,
pubmed-meshheading:3100638-T-Lymphocytes
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pubmed:year |
1987
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pubmed:articleTitle |
Modulation of CD4 by antigenic activation.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|