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International Immunology Advance Access originally published online on November 29, 2004
International Immunology 2005 17(1):55-63; doi:10.1093/intimm/dxh185
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© 2005 The Japanese Society for Immunology

Pregnancy-induced alterations of B cell maturation and survival are differentially affected by Fas and Bcl-2, independently of BcR expression

Stéphane M. Caucheteux1, Marie-Claude Gendron2 and Colette Kanellopoulos-Langevin1

1 Laboratory of Immune Regulations and Development, Department of Developmental Biology and 2 Flow Cytometry Unit, Institut J. Monod, UMR 7592 (CNRS and Universities Paris 6 and 7), 2 place Jussieu, 75251 Paris cedex 05, France

Correspondence to: C. Kanellopoulos-Langevin; E-mail: kanellopoulos{at}ijm.jussieu.fr

In the present work, we have analyzed the roles of two molecules involved in the regulation of cell survival, Bcl2 and Fas, in the pregnancy-induced down-regulation of B lymphopoiesis in mice. Our results show that the overexpression of the anti-apoptotic molecule Bcl2 in Bcl2-transgenic (Tg) B cells is able to protect ‘D’ fraction pre-B cells from pregnancy-induced deletion. In contrast, in Faslpr/lpr mice bearing a mutated cell death receptor Fas, such B cell targets are not protected. Moreover, bone marrow B cell sub-populations at both ends of the differentiation pathway, i.e. pre-pro ‘A’ and mature ‘E–F’ fraction B cells, which are not the major targets of the pregnancy-induced down-regulation, are doubled during pregnancy in Faslpr/lpr mice only. Altogether, these data strongly suggest that B cell down-regulation during pregnancy is due to apoptotic events blocked by Bcl2, but does not depend on a functional Fas receptor. The expression of a transgenic BcR in the 3-83µ{delta} BcR-Tg mouse model yields similar observations, which indicates that early BcR expression does not alter bone marrow B cell fates during pregnancy.

Keywords: apoptosis, B lymphocytes, Lupus, mice, pregnancy

Transmitting editor: P. Kincade


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