Abstract
BAFF is an essential cytokine primarily known for its role in maintaining B cell homeostasis via induction of a pro-survival gene expression profile. Additionally, recent evidence suggests that BAFF induced signaling also drives a metabolic program that is needed for homeostatic cell mass maintenance in resting B cells and which increases the cells' capacity to divide. Many components of the signaling cascades initiated by BAFF, the alternative NFκB pathway and the PI3K/AKT/mTOR pathway, are active in roles beyond their classically assigned function. These components can directly or indirectly impact metabolic reprogramming. Further exploration of the role BAFF signaling plays in B cell metabolism could help to identify metabolic vulnerabilities of hyperactive B cells in the context of autoimmunity.
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