A p56(lck)-independent pathway of CD2 signaling involves Jun kinase

Abstract

The p56(lck) Src family non-receptor tyrosine kinase has been shown to be critical for T lymphocyte differentiation and activation. Hence in the absence of p56(lck), 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(lck). CD2-mediated interleukin-2 production occurs via activation of Jun kinase in cell lines lacking p56(lck). 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.