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The Journal of Immunology, Vol 159, Issue 4 1639-1647, Copyright © 1997 by American Association of Immunologists
ARTICLES |
MA Musci, DG Motto, SE Ross, N Fang and GA Koretzky
Graduate Program in Immunology, University of Iowa College of Medicine, Iowa City 52242, USA.
We and others have shown that overexpression of SLP-76 augments TCR- stimulated IL-2 promoter activity in the Jurkat T cell line. In this report we investigate the signaling mechanisms through which SLP-76 mediates its effect on T cell activation. We show that overexpressed SLP-76 acts downstream of TCR-stimulated protein tyrosine kinases, but does not affect calcium signaling. Overexpression of SLP-76 does, however, augment TCR stimulation of both ERK (extracellular signal- regulated kinase) activity and a reporter construct driven by activating protein-1 binding sites. Structure/function analysis reveals that three distinct regions of SLP-76, each important for protein associations, are required for augmentation of TCR-induced nuclear factor-AT activity. These data suggest that SLP-76 functions as an adapter molecule that requires three unique domains to link proximal TCR signals in T cells.
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