A p56lck-independent Pathway of CD2 Signaling Involves Jun Kinase

• 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
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1074/jbc.273.37.24249

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.