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. JEM © The Rockefeller University Press.
Patke, A., Mecklenbräuker, I., Erdjument-Bromage, H., Tempst, P., & Tarakhovsky, A. (2006). BAFF controls B cell metabolic fitness through a PKCβ- and Akt-dependent mechanism. Journal of Experimental Medicine, 203(11), 2551–2562. https://doi.org/10.1084/jem.20060990