JNK, but not MAPK, activation is associated with Fas-mediated apoptosis in human T cells

✍ Scribed by David J. Wilson; Karen A. Fortner; David H. Lynch; Raymond R. Mattingly; Ian G. Macara; James A. Posada; Ralph C. Budd

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 680 KB
• Volume: 26
• Category: Article
• ISSN: 0014-2980
• DOI: 10.1002/eji.1830260505

✦ Synopsis

JNK, but not MAPK, activation is associated with Fas-mediated apoptosis in human T cells

Fas is a cell surface molecule that is expressed on a wide array of cell types and triggers apoptosis. While in most situations Fas ligation activates programmed cell death, on resting T lymphocytes it can co-stimulate proliferation with the T cell receptor (TCR)/CD3 complex. This incongruity suggests that Fas may elicit signaling events that overlap with those used by proliferation cues. We observe that in the human T cell line Jurkat and in human peripheral blood lymphocytes, Fas stimulation does not signal by the Ras/Raf-l/mitogen-activated protein kinase (MAPK) pathway or by increased intracellular calcium. Rather, Fas ligation strongly activates Jun kinase (JNK). This activity, as well as Fas-induced apoptosis, is blocked by increased levels of CAMP. The balance between proliferation and apoptosis by Fas triggering of T lymphocytes may therefore reflect a signaling ratio between TCR activation of the RadRaf-l/MAPK pathway versus JNK activation by Fas.