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Journal Article

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

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Leitges,  M.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

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Citation

Mecklenbraeuker, I., Kalled, S. L., Leitges, M., Mackay, F., & Tarakhovsky, A. (2004). Regulation of B-cell survival by BAFF-dependent PKCdelta-mediated nuclear signalling. Nature, 431(7007), 456-461. Retrieved from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15361883.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-EC32-4
Abstract
Approximately 65% of B cells generated in human bone marrow are potentially harmful autoreactive B cells. 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 cells. Escape of self-reactive B cells from tolerance permits production of pathogenic auto-antibodies; recent studies suggest that extended B lymphocyte survival is a cause of autoimmune disease in mice and humans. Here we report a mechanism for the regulation of peripheral B-cell survival by serine/threonine protein kinase Cdelta (PKCdelta): spontaneous death of resting B cells is regulated by nuclear localization of PKCdelta 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 PKCdelta. Our data suggest the existence of a previously unknown BAFF-induced and PKCdelta-mediated nuclear signalling pathway which regulates B-cell survival.