The Journal of Experimental Medicine
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Published online 23 October 2006 doi:10.1084/jem.20060990
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 11, 2551-2562
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ARTICLE

 BAFF controls B cell metabolic fitness through a PKCß- and Akt-dependent mechanism

Alina Patke1, Ingrid Mecklenbräuker1, Hediye Erdjument-Bromage2, Paul Tempst2, and Alexander Tarakhovsky1

1 Laboratory of Lymphocyte Signaling, The Rockefeller University, New York, NY 10021
2 Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021

CORRESPONDENCE Alina Patke: patkea{at}mail.rockefeller.edu OR Alexander Tarakhovsky: tarakho{at}mail.rockefeller.edu

B cell life depends critically on the cytokine B cell–activating factor of the tumor necrosis factor family (BAFF). Lack of BAFF signaling leads to B cell death and immunodeficiency. Excessive BAFF signaling promotes lupus-like autoimmunity. Despite the great importance of BAFF to B cell biology, its signaling mechanism is not well characterized. We show that BAFF initiates signaling and transcriptional programs, which support B cell survival, metabolic fitness, and readiness for antigen-induced proliferation. We further identify a BAFF-specific protein kinase C ß–Akt signaling axis, which provides a connection between BAFF and generic growth factor–induced cellular responses.

Abbreviations used: 4E-BP1, eIF4E-binding protein 1; BCR, B cell antigen receptor; BAFF, B cell–activating factor of the TNF family; BAFF-R, BAFF receptor; eIF4E, eukaryotic translation initiation factor 4E; GO, gene ontology; GSK-3, glycogen synthase kinase–3; PI3K, phosphoinositide 3–kinase; PKCß and PKC{delta}, protein kinase C ß and {delta}, respectively; PTEN, phosphatase and tensin homologue deleted on chromosome 10; TMRE, tetramethylrhodamine ethyl ester; TSC2, tuberous sclerosis complex 2.


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