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

J Exp Med. 2006 Oct 30;203(11):2551-62. doi: 10.1084/jem.20060990. Epub 2006 Oct 23.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B-Cell Activating Factor / physiology*
  • B-Lymphocytes / enzymology
  • B-Lymphocytes / metabolism*
  • Cell Proliferation
  • Cell Survival / immunology
  • Cells, Cultured
  • Mice
  • Protein Kinase C / deficiency
  • Protein Kinase C / genetics
  • Protein Kinase C / physiology*
  • Protein Kinase C beta
  • Proto-Oncogene Proteins c-akt / physiology*
  • Signal Transduction / immunology


  • B-Cell Activating Factor
  • Tnfsf13b protein, mouse
  • Proto-Oncogene Proteins c-akt
  • Protein Kinase C
  • Protein Kinase C beta