Interferon-α induction of STATs1, -3 DNA binding and growth arrest is independent of Lck and active mitogen-activated kinase in T cells

Troy C. Lund, Maria M. Medveczky, Peter G. Medveczky

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Type I interferons (IFNs) are a family of cytokines that have antiviral and antiproliferative effects. Data regarding the processes by which these cytokines transduce signals from the cell membrane to the nucleus are becoming increasingly complex. The most characterized pathway is via JAK- STAT signaling. Previous studies established a potential role for the Src- family kinase Lck in JAK-STAT signaling. Therefore, this study was designed to analyze the role of Lck in IFN-α signaling by using the Jurkat, JCam (an Lck-defective cell line derived from Jurkat), and JCam/Lck (JCam cells with Lck restored). The results show that IFN-α can induce MAPK activity, but only in cells containing Lck. Furthermore, STATs1 and -3 are effectively phosphorylated and activated to bind DNA in the absence of Lck expression in IFN-α-treated cells. Finally, the results demonstrate that IFN-α exerts an antiproliferative effect in all three cell lines. These data indicate that Lck and active MAPK do not affect IFN-α-induced growth arrest or induction of STAT1s1 and -3 DNA binding ability.

Original languageEnglish (US)
Pages (from-to)133-139
Number of pages7
JournalCellular Immunology
Volume192
Issue number2
DOIs
StatePublished - Mar 15 1999
Externally publishedYes

Keywords

  • Cytokines
  • Molecular biology
  • Signal transduction
  • T lymphocytes

Fingerprint Dive into the research topics of 'Interferon-α induction of STATs1, -3 DNA binding and growth arrest is independent of Lck and active mitogen-activated kinase in T cells'. Together they form a unique fingerprint.

Cite this