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Letters to Nature
Nature 431, 456-461 (1 September 2004) | doi:10.1038/nature02955; Received 12 July 2004; Accepted 16 August 2004; Published online 8 September 2004
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Regulation of B-cell survival by BAFF-dependent PKC
-mediated nuclear signalling
Ingrid Mecklenbräuker1, Susan L. Kalled2, Michael Leitges3, Fabienne Mackay4 & Alexander Tarakhovsky1
- Laboratory of Lymphocyte Signaling, The Rockefeller University, New York, New York 10021, USA
- Biogen Idec, Inc., Cambridge, Massachusetts 02142, USA
- Max Planck Institute for Experimental Endocrinology, D 30625 Hannover, Germany
- Garvan Institute of Medical Research, St Vincent Hospital, Darlinghurst, NSW 2010, Sydney, Australia
Correspondence to: Alexander Tarakhovsky1 Email: tarakho@mail.rockefeller.edu
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 C
(PKC
): spontaneous death of resting B cells is regulated by nuclear localization of PKC
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 PKC
. Our data suggest the existence of a previously unknown BAFF-induced and PKC
-mediated nuclear signalling pathway which regulates B-cell survival.
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