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International Immunology Advance Access published online on March 15, 2007
International Immunology, doi:10.1093/intimm/dxm011
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

The role of BLyS/BLyS receptors in anti-chromatin B cell regulation

Brian D. Hondowicz1, Shawn T. Alexander1, William J. Quinn, III2, Antonio J. Pagán1, Michele H. Metzgar1, Michael P. Cancro2 and Jan Erikson1

1 The Wistar Institute, Room 276, 3601 Spruce Street, Philadelphia, PA 19104, USA
2 Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA

Correspondence to: Correspondence to: J. Erikson; E-mail: jan{at}wistar.org

B lymphocyte stimulator (BLyS), also known as B cell-activating factor, is a key positive regulator of B cell homeostasis, and elevated levels of BLyS have been observed in systemic lupus erythematosus (SLE) patients. Given that anti-chromatin auto-antibodies are one of the hallmarks of SLE, we examined the role of BLyS and its receptors in the regulation of anti-chromatin B cells. We demonstrate that exogenous BLyS treatment leads to an increase in B cell numbers, particularly anti-chromatin B cells; yet, their localization in the spleen and auto-antibody production remain unaffected. We also examined transmembrane activator and CAML interactor (TACI), BLyS receptor 3 (BR3) and B cell maturation antigen expression on anti-chromatin B cells before and after receiving T cell help. Interestingly, in the absence of T cell help, TACI expression is greater on immature anti-chromatin B cells compared with immature Tg(–) B cells, whereas BR3 levels are comparable. After receiving T cell help, the anti-chromatin B cells that have differentiated into short-lived plasma cells no longer express BR3 but retain TACI. These data suggest a novel role for TACI in anti-chromatin B cell homeostasis and differentiation.

Keywords: auto-antibody, autoimmunity, cytokines

Transmitting editor: C. Goodnow

Received 21 August 2006, accepted 19 January 2007.


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