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B Couples Protein Kinase B/Akt Signaling to Distinct Survival Pathways and the Regulation of Lymphocyte Homeostasis In Vivo
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* Department of Medical Biophysics and
Department of Immunology,
Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University of Toronto, Toronto, Ontario, Canada;
Walter and Eliza Hall Institute of Medical Research, Parkville, Australia; and
¶ Department of Microbiology and Immunology, Vanderbilt University Medical School, Nashville TN 37232
Protein kinase B (PKB
/Akt1) a PI3K-dependent serine-threonine kinase, promotes T cell viability in response to many stimuli and regulates homeostasis and autoimmune disease in vivo. To dissect the mechanisms by which PKB inhibits apoptosis, we have examined the pathways downstream of PKB that promote survival after cytokine withdrawal vs Fas-mediated death. Our studies show that PKB-mediated survival after cytokine withdrawal is independent of protein synthesis and the induction of NF-
B. In contrast, PKB requires de novo gene transcription by NF-B to block apoptosis triggered by the Fas death receptor. Using gene-deficient and transgenic mouse models, we establish that NF-B1, and not c-Rel, is the critical signaling molecule downstream of the PI3K-PTEN-PKB signaling axis that regulates lymphocyte homeostasis.
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