BAFF controls B cell metabolic fitness through a PKC beta- and Akt-dependent mechanism.
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.
Patke
Alina
A
Laboratory of Lymphocyte Signaling, The Rockefeller University, New York, NY 10021, USA. patkea@mail.rockefeller.edu
Mecklenbräuker
Ingrid
I
Erdjument-Bromage
Hediye
H
Tempst
Paul
P
Tarakhovsky
Alexander
A
D000818:Animals; D053264:B-Cell Activating Factor / Q000502:physiology*; D001402:B-Lymphocytes / Q000201:enzymology / Q000378:metabolism*; D049109:Cell Proliferation; D002470:Cell Survival / Q000276:immunology; D002478:Cells, Cultured; D051379:Mice; D011493:Protein Kinase C / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D064546:Protein Kinase C beta; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology
D053264:B-Cell Activating Factor; C505720:Tnfsf13b protein, mouse; D051057:Proto-Oncogene Proteins c-akt; D011493:Protein Kinase C; D064546:Protein Kinase C beta