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International Immunology Advance Access published online on November 20, 2007
International Immunology, doi:10.1093/intimm/dxm116
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Tolerance induction to self-MHC antigens in fetal and neonatal mouse B cells

Stéphane M. Caucheteux1,2,*, Cécile Vernochet1,*, Josiane Wantyghem1, Marie-Claude Gendron3 and Colette Kanellopoulos-Langevin1

1 Laboratory of Immune Regulations and Development, Department of Developmental Biology, J. Monod Institute, UMR 7592 (CNRS and Universities Paris 6 and 7), 2 place Jussieu, 75251 Paris cedex 05, France
2 Present address: Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
3 Flow Cytometry Unit, J. Monod Institute, 75251 Paris cedex 05, France

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

We have studied the mechanisms of tolerance induction to self-MHC antigens in mouse B cells during fetal development and the post-natal period. To monitor the fate of autoreactive B cell clones, we used the 3-83µ{delta} B cell receptor (BCR)-transgenic (Tg) and -knock-in (KI) mouse models. These BCR-Tg and -KI B cells recognize the MHC class I molecules H-2Kk and H-2Kb, with a high or moderate affinity, respectively. We compared the fate of BCR-Tg and -KI B cells in H-2Kb-bearing animals and H-2Kb-negative controls at various stages of their fetal development and post-natal life. Our data show that, in contrast to what occurs in adult B cells, anergy is the main component of tolerance induction in 3-83µ{delta} BCR-Tg Kb+ autoreactive fetuses, while 3-83 BCR-KI fetuses primarily use receptor editing. Interestingly, autoreactive B cell deletion is absent or merely marginal before birth. Our results indicate that tolerance induction is effective as early as embryonic day 16.5 and that in the fetus and neonate, like in the adult, the main mechanism of B cell tolerance functioning in the 3-83 KI system is receptor editing. In contrast, in the 3-83µ{delta} mice where receptor editing is hindered, adult and fetal B cells differ in their preferential use of mechanisms leading to self-tolerance (i.e. deletion versus anergy).

Keywords: B cells, MHC, tolerance/anergy, transgenic mice

* These authors contributed equally to this work.

Transmitting editor: A. Radbruch

Received 6 November 2006, accepted 10 October 2007.


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