Abstract
Signalling through the IFNalphaR (interferon-alpha receptor) and TCR (T-cell receptor) in Jurkat T lymphocytes results in distinct immune responses. Despite this both receptors elicit ERK (extracellular-signal-regulated kinase)/MAPK (mitogen-activated protein kinase) phosphorylation. Vav and Slp76 are shown to be required for IFNalpha (interferon-alpha)-stimulated ERK activity. These form a subset of proteins which behave identically on stimulation of both receptors. TCR deletion abrogates IFNalphaR-stimulated MAPK activity, whereas the canonical JAK/STAT (Janus kinase/signal transducer and activator of transcription) pathway is unaffected. Thus recruitment of the intact TCR ESC (early signalling complex) is necessary for this downstream MAPK response. Despite using a common ESC, stimulation of the IFNalphaR does not produce the transcriptional response associated with TCR. Up-regulation of the MAPK pathway by IFNalphaR might be important to ensure that the cell responds to only one stimulant.