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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1997-1-15
|
| pubmed:abstractText |
The present study has examined the role of IL-2 and IL-4 in the regulation of different kinase pathways for the generation of alphaCD3-induced activated killer cells, CD3-AK. It has previously been shown that the IL-2 promoted CD3-AK cell response is mediated through a PKC (protein kinase C)-dependent pathway, which is susceptible to PKC inhibitors and resistant to inhibitors of PTK (protein tyrosine kinase), and that IL-4 synergized with IL-2 to induce CD3-AK cells. However, the IL-4-promoted CD3-AK cell response was PKC-independent as assessed by its resistance to PKC inhibitors. These findings suggest a dichotomy in the pathways leading to CD3-AK cell generation. To further determine whether IL-4 mediated a different kinase pathway to activate the T cells, we studied its effect on protein tyrosine phosphorylation. IL-4 up-regulated protein tyrosine phosphorylation in CD3-AK cells in a dose-dependent fashion, and resulted in increased levels of a number of phosphorylated proteins. Of particular note was the increase of tyrosine phosphorylated p56(lck) and p59(fyn) in CD3-AK cells. The changes in global protein tyrosine phosphorylation were correlated with the up-regulation by IL-4 of CD3-AK cell cytolytic activity, and the production of granzyme A. alphaIL-4 specifically blocked all the effects which were induced by IL-4. The PTK inhibitor genistein inhibited the IL-4-augmented cytolytic activity of CD3-AK cells as well as the IL-4-induced augmentation of protein tyrosine phosphorylation to the basal level of CD3-AK cells cultured in IL-2 alone. Consistent with a dichotomy in pathways for IL-2- and IL-4-mediated CD3-AK generation, genistein had no effect on the generation of CD3-AK cells cultured in IL-2 alone. Thus while PKC is primarily involved in the generation of IL-2-promoted CD3-AK cells, PTK appears to be required for the regulation of IL-4-promoted CD3-AK response.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Genistein,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Isoflavones,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0008-8749
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
174
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
138-46
|
| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading |
pubmed-meshheading:8954613-Animals,
pubmed-meshheading:8954613-Antigens, CD3,
pubmed-meshheading:8954613-Cytotoxicity, Immunologic,
pubmed-meshheading:8954613-Enzyme Inhibitors,
pubmed-meshheading:8954613-Female,
pubmed-meshheading:8954613-Genistein,
pubmed-meshheading:8954613-Immunophenotyping,
pubmed-meshheading:8954613-Interleukin-1,
pubmed-meshheading:8954613-Interleukin-4,
pubmed-meshheading:8954613-Isoflavones,
pubmed-meshheading:8954613-Killer Cells, Lymphokine-Activated,
pubmed-meshheading:8954613-Lymphocyte Activation,
pubmed-meshheading:8954613-Mice,
pubmed-meshheading:8954613-Mice, Inbred C57BL,
pubmed-meshheading:8954613-Phosphorylation,
pubmed-meshheading:8954613-Protein Kinase C,
pubmed-meshheading:8954613-Protein Kinase Inhibitors,
pubmed-meshheading:8954613-Protein Kinases,
pubmed-meshheading:8954613-Signal Transduction,
pubmed-meshheading:8954613-Tumor Cells, Cultured,
pubmed-meshheading:8954613-Tyrosine
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
IL-2 and IL-4 mediate through two distinct kinase pathways for the activation of alphaCD3-induced activated killer cells.
|
| pubmed:affiliation |
Laboratory of Immune Cell Biology, Division of Basic Science, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
|
| pubmed:publicationType |
Journal Article
|