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

Alina Patke,Ingrid Mecklenbräuker,H. Erdjument‐Bromage,P. Tempst,A. Tarakhovsky

Published 2006 in Journal of Experimental Medicine

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 β–Akt signaling axis, which provides a connection between BAFF and generic growth factor–induced cellular responses.

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