Regulation of B-cell survival by BAFF-dependent PKCδ-mediated nuclear signalling

Ingrid Mecklenbräuker, Susan L. Kalled, Michael Leitges, Fabienne Mackay and Alexander Tarakhovsky ()
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Ingrid Mecklenbräuker: The Rockefeller University
Susan L. Kalled: Biogen Idec, Inc.
Michael Leitges: Max Planck Institute for Experimental Endocrinology
Fabienne Mackay: St Vincent Hospital, Darlinghurst
Alexander Tarakhovsky: The Rockefeller University

Nature, 2004, vol. 431, issue 7007, 456-461

Abstract: Abstract Approximately 65% of B cells generated in human bone marrow are potentially harmful autoreactive B cells1. Most of these cells are clonally deleted in the bone marrow, while those autoreactive B cells that escape to the periphery are anergized or perish before becoming mature B cells2,3,4,5. Escape of self-reactive B cells from tolerance permits production of pathogenic auto-antibodies6; recent studies suggest that extended B lymphocyte survival is a cause of autoimmune disease in mice and humans7. Here we report a mechanism for the regulation of peripheral B-cell survival by serine/threonine protein kinase Cδ (PKCδ): spontaneous death of resting B cells is regulated by nuclear localization of PKCδ that contributes to phosphorylation of histone H2B at serine 14 (S14-H2B). We show that treatment of B cells with the potent B-cell survival factor BAFF (‘B-cell-activating factor belonging to the TNF family’) prevents nuclear accumulation of PKCδ. Our data suggest the existence of a previously unknown BAFF-induced and PKCδ-mediated nuclear signalling pathway which regulates B-cell survival.

Date: 2004
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DOI: 10.1038/nature02955

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