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

17Citations
Citations of this article
58Readers
Mendeley users who have this article in their library.

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. JEM © The Rockefeller University Press.

Cite

CITATION STYLE

APA

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

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free