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The Journal of Immunology, 1998, 161: 3416-3420.
Copyright © 1998 by The American Association of Immunologists

Impaired TCR-Mediated Apoptosis and Bcl-XL Expression in T Cells Lacking the Stress Kinase Activator SEK1/MKK4

Hiroshi Nishina*,§,¶, Laszlo Radvanyi§,¶, Kaliannan Raju§,¶, Takehiko Sasaki*,§,¶, Ivona Kozieradzki*,§,¶ and Josef M. Penninger1,*,§,¶

* Amgen Institute, University of Toronto, Ontario, Canada; and {dagger} Ontario Cancer Institute, and {ddagger} Departments of Medical Biophysics and Immunology, University of Toronto, Ontario, Canada; and § Ontario Cancer Institute, Departments of Medical Biophysics and Immunology, Ontario, Canada.

The dual specificity kinase SEK1 (MKK4) is a direct activator of stress-activated protein kinases (SAPK/JNK) in response to environmental stresses or mitogenic factors. We show in Sek1-/-Rag-/- chimeric mice that a Sek1 null mutation augments the susceptibility of peripheral T cells to TCR/CD3 religation-induced apoptosis. Sek1-/- T cells failed to induce expression of the death suppressor Bcl-XL in response to Ag receptor activation. The Sek1 mutation did not alter the induction of apoptosis in response to etoposide, cisplatinum, Adriamycin, and {gamma}-irradiation. Moreover, we show that CD3{epsilon} activation alone leads to SEK1 activation in Sek1+/+ T cells. These results suggest that SEK1 transduces cellular survival signals during T cell stimulation.




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