Antiproliferative action of interferon-α requires components of T- cell-receptor signalling

E. F. Petricoin, S. Ito, B. L. Williams, S. Audet, L. F. Stancato, A. Gamero, K. Clouse, P. Grimley, A. Weiss, J. Beeler, D. S. Finbloom, E. W. Shores, R. Abraham, A. C. Larner*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

141 Scopus citations


Signal transduction through both cytokine and lymphocyte antigen receptors shares some common pathways by which they initiate cellular responses, such as activation of mitogen-activated protein kinase(s). However, other signalling components appear to be uniquely coupled to each receptor. For example, the interferon receptors transduce regulatory signals through the JAK/STAT pathway, resulting in an inhibition of growth and of antiviral effects, whereas this pathway apparently plays no role in T-cell- receptor (TCR)-dependent gene expression. Conversely, signal transduction through the TCR requires the tyrosine kinases Lck and ZAP-70 and the tyrosine phosphatase CD45 (ref. 5). Here we show that, unexpectedly, transmission of growth-inhibitory signals by interferon-α (IFN-α) in T cells requires the expression and association of CD45, Lck and ZAP-70 with the IFN-α-receptor signalling complex.

Original languageEnglish
Pages (from-to)629-632
Number of pages4
Issue number6660
StatePublished - 1997
Externally publishedYes


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