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Published on: May 16, 2021
BAFF controls B cell metabolic fitness through a PKC beta- and Akt-dependent mechanism
Alina Patke1, Ingrid Mecklenbräuker, Hediye Erdjument-Bromage
1Laboratory of Lymphocyte Signaling, The Rockefeller University, New York, NY 10021, USA. patkea@mail.rockefeller.edu
Abstract:
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 beta-Akt signaling axis, which provides a connection between BAFF and generic growth factor-induced cellular responses.
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