A p56lck-independent Pathway of CD2 Signaling Involves Jun Kinase

The p56 Src family non-receptor tyrosine kinase has been shown to be critical for T lymphocyte differentiation and activation. Hence in the absence of p56, T cell receptor triggered activation does not occur. We now provide evidence for a CD2-based signaling pathway which, in contrast to that of the...

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Bibliographic Details
Published in:The Journal of biological chemistry 1998-09, Vol.273 (37), p.24249-24257
Main Authors: Sunder-Plassmann, Raute, Reinherz, Ellis L.
Format: Article
Language:English
Subjects:
Antigens, CD - physiology
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
CD2 Antigens - physiology
Cell Differentiation
Humans
Interleukin-2 - biosynthesis
Interleukin-2 - genetics
JNK Mitogen-Activated Protein Kinases
Jurkat Cells - cytology
Jurkat Cells - immunology
Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - deficiency
Lymphocyte Specific Protein Tyrosine Kinase p56(lck) - metabolism
Mitogen-Activated Protein Kinases
Models, Immunological
Phosphorylation
Phosphotyrosine - analysis
Promoter Regions, Genetic
Receptors, Antigen, T-Cell - physiology
Signal Transduction
T-Lymphocytes - cytology
T-Lymphocytes - immunology
Transcription Factor AP-1 - metabolism
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Summary:The p56 Src family non-receptor tyrosine kinase has been shown to be critical for T lymphocyte differentiation and activation. Hence in the absence of p56, T cell receptor triggered activation does not occur. We now provide evidence for a CD2-based signaling pathway which, in contrast to that of the T cell receptor, is independent of p56. CD2-mediated interleukin-2 production occurs via activation of Jun kinase in cell lines lacking p56. Jun kinase then facilitates the binding of c-Jun/c-Fos heterodimers to the AP-1 consensus site and the subsequent transcriptional activity of the interleukin-2 promoter. These data elucidate differences between TCR and CD2 signaling pathways in the same T cells.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.273.37.24249